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129 publications mentioning hsa-mir-212 (showing top 100)

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-212. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 454
A. The FOXA1 expression plasmid significantly upregulated the expression of FOXA1 in miR-212 overexpressing HepG2 cells (HepG2-miR-212), while FOXA1 specific siRNA effectively downregulated FOXA1 expression in Bel-7402 cells transfected with miR-212 inhibitors (Bel-7402-anti-miR-212). [score:17]
Figure 5 A. The FOXA1 expression plasmid significantly upregulated the expression of FOXA1 in miR-212 overexpressing HepG2 cells (HepG2-miR-212), while FOXA1 specific siRNA effectively downregulated FOXA1 expression in Bel-7402 cells transfected with miR-212 inhibitors (Bel-7402-anti-miR-212). [score:17]
Up-regulation of miR-212 significantly reduced the expression of FOXA1 in HepG2 cells, whereas down-regulation of miR-212 increased the expression of FOXA1 in Bel-7402 cells. [score:11]
FOXA1 expression was significantly up-regulated in HepG2-miR-212 cells after FOXA1 plasmid transfection, and resulted in obvious up-regulation of YAP and AFP (P < 0.01, respectively, Figure 5A). [score:9]
C. Up-regulation of miR-212 in HepG2 cells significantly inhibited the expression of FOXA1, AFP and YAP. [score:8]
Our data confirmed that miR-212 down-regulated YAP expression by inhibiting FOXA1. [score:8]
A. MiR-212 mimics significantly increased the expression of miR-212, while miR-212 inhibitors effectively decreased miR-212 expression, as determined by qRT-PCR. [score:7]
To further determine whether FOXA1 is a functional target of miR-212, we restored the FOXA1 expression in HepG2-miR-212 cells by transfecting FOXA1 expression plasmid. [score:7]
MiR-212 inhibits HCC cell proliferation and induces apoptosis in vitro and in vivoTo further explore the biological role of miR-212 in HCC, a miR-212 expression vector and a miR-212 inhibitor (anti-miR-212) was transfected into HepG2 and Bel-7402 cells, respectively. [score:7]
The expression of AFP and YAP, the downstream targets of FOXA1, were reduced accordingly in miR-212 overexpressing HepG2 cells (P < 0.01, respectively, Figure 4C). [score:7]
Figure 2 A. MiR-212 mimics significantly increased the expression of miR-212, while miR-212 inhibitors effectively decreased miR-212 expression, as determined by qRT-PCR. [score:7]
As presented in Figure 4B, the expression of FOXA1 in miR-212 high -expressing HCC tissues was significantly lower than that in miR-212 low -expressing cases (P < 0.01). [score:7]
MiRNA vectors, including miR-212 expression vector (HmiR0269-MR04), the control vector for miR-212 (CmiR0001-MR04), miR-212 inhibitor (HmiR-AN0319-AM04) and the negative control for the miR-212 inhibitor (CmiR-AN0001-AM04), were purchased from Genecopoeia (Guangzhou, China). [score:7]
B. Up-regulation of miR-212 inhibited proliferation and induced apoptosis in vivo. [score:6]
In contrast, down-regulation of miR-212 resulted in increased expression of FOXA1, AFP and YAP in Bel-7402 cells (P < 0.01, respectively, Figure 4C). [score:6]
Down-regulation of miR-212 in Bel-7402 cells significantly increased the expression of FOXA1, AFP and YAP. [score:6]
Herein, we performed dual-luciferase reporter gene assays to determine whether miR-212 could directly target 3′-UTR of FOXA1 mRNA to regulate its expression. [score:6]
The expression of miR-212 is down-regulated in HCC tissues and cell lines. [score:6]
In conclusion, we find that miR-212 is down-regulated in HCC and its decreased expression is associated with poor prognostic features. [score:6]
As expected, miR-212 significantly inhibited the luciferase activity of FOXA1 containing a wild-type (wt) 3′-UTR but did not suppress activity of FOXA1 with a mutant (mt) 3′-UTR (P < 0.01, Figure 4D). [score:5]
Therefore, comparing the advantage of miR-212 targeted therapies to conventional and targeted drugs (e. g. sorafenib) for HCC will be of great importance in further study. [score:5]
In contrast, HCC patients with high expression of miR-212 and low expression of FOXA1 had the best OS and DFS (Figure 6E and 6F). [score:5]
To find out the molecular mechanism responsible for the biological functions of miR-212 in HCC cells, we searched for candidate target genes of miR-212 by using public databases including TargetScan (http://www. [score:5]
Mechanistically, we suggest that miR-212 inhibits HCC cell viability and proliferation, and induces apoptosis by suppressing FOXA1. [score:5]
Our data confirmed that forced expression of miR-212 inhibited cell proliferation and induced apoptosis in vivo (P < 0.01, respectively, Figure 3B). [score:5]
Taken together, these data provide solid evidences to support that miR-212 exerts it inhibitory effect on HCC, at least in part, through inhibiting FOXA1. [score:5]
In vitro and in vivo studies indicate that miR-212 inhibits tumor growth by inhibiting HCC cell proliferation and promoting apoptosis. [score:5]
Overexpression of miR-212 in HepG2 cells dramatically reduced the expression of FOXA1 (P < 0.01, Figure 4C). [score:5]
Moreover, two public databases (TargetScan and Miranda) facilitated us to find out that FOXA1 was one of the predicted targets of miR-212. [score:5]
Then, HepG2 cells (1 × 10 [5]) were seeded into 24-well plates, and were cultured in OptimMEM reduced serum media (Life Technologies) as per the recommended conditions, and were cotransfected with 200 ng of each luciferase reporter construct (the wt or mt 3′-UTR of FOXA1 mRNA) and miR-212 expression vector, miR-212 inhibitor, control vector or negative control (50 nM) using Fugene (Promega, Madison, WI, USA). [score:5]
Moreover, we revealed that miR-212 exerted its biological function, at least in part, by inhibiting FOXA1 expression. [score:5]
Figure 6HCC patients with high expression of miR-212 had better A. overall survival (OS) and B. disease free survival (DFS). [score:5]
Figure 3 A. Tumor growth curve revealed that miR-212 overexpression significantly inhibited tumor growth in vivo. [score:5]
A. Tumor growth curve revealed that miR-212 overexpression significantly inhibited tumor growth in vivo. [score:5]
To further explore the biological role of miR-212 in HCC, a miR-212 expression vector and a miR-212 inhibitor (anti-miR-212) was transfected into HepG2 and Bel-7402 cells, respectively. [score:5]
Moreover, as determined by flow cytometry and caspase 3/7 activity assays, miR-212 overexpression increased the percentage of apoptotic HepG2 cells (P < 0.01, for both assays, Figure 2D and 2E) and its down-regulation inhibited apoptosis in Bel-7402 cells (P < 0.01, for both assays, Figure 2D and 2E). [score:5]
Patients with low expression of miR-212 and high expression of FOXA1 had the lowest OS and DFS (Figure 6E and 6F). [score:5]
D. miR-212 overexpression significantly suppressed the luciferase activity that carried wild type but not mutant type 3′-UTR of FOXA1. [score:5]
Our study indicated that miR-212 decreased the expression of AFP by inhibiting FOXA1. [score:5]
This finding suggests that FOXA1, an important regulator of cell proliferation and apoptosis, may be a direct downstream target of miR-212. [score:5]
Our results elucidate the underlying mechanism by which miR-212 inhibits HCC, and propose miR-212 as a potential therapeutic target for HCC. [score:5]
FOXA1 is a direct downstream target of miR-212. [score:4]
To determine the expression status of miR-212 in HCC, we initially compared the expression of miR-212 in 40 pairs of HCC tissues and adjacent non-tumor tissues. [score:4]
In this study, we found that miR-212 was down-regulated in the majority of HCC tissues. [score:4]
Compared with patients with high level of miR-212, patients with low expression of miR-212 had shorter overall survival (OS) (P = 0.002, Figure 6A) and disease free survival (DFS) (P < 0.001, Figure 6B). [score:4]
In this study, we confirmed that FOXA1 was a direct downstream target of miR-212 and it was implicated in the functional effect of miR-212 on HCC. [score:4]
FOXA1 is a direct downstream target of miR-212 in HCC. [score:4]
Downregulating miR-212 increased the luciferase activity that carried wild type but not mutant type 3′-UTR of FOXA1. [score:4]
Tumor growth curves, generated over 21 days, revealed that up-regulation of miR-212 significantly slowed down tumor growth in mice (P < 0.01, Figure 3A). [score:4]
MTT and BrdU assays demonstrated that forced expression of miR-212 in HepG2 cells (HepG2-miR-212) resulted in significant decrease of cell viability and proliferation (P < 0.01, respectively, Figure 2B and 2C), while down-regulation of miR-212 in Bel-7402 cells (Bel-7402-anti-miR-212) showed remarkable increase of cell viability and proliferation as compared with control cells (P < 0.01, respectively, Figure 2B and 2C). [score:4]
Altering FOXA1 expression partly abrogated the effect of miR-212 on HCC cells. [score:3]
These results indicate that miR-212 adversely affects tumor growth of HCC by inhibiting cell viability and proliferation, and inducing apoptosis. [score:3]
5 × 10 [6] HepG2 cells transfected with miR-212 expressing or control vectors were mixed in 150 uL of Matrigel and were inoculated subcutaneously into the flank of nude mouse. [score:3]
The relative expression of miR-212 was shown as fold difference relative to U6. [score:3]
Interestingly, we confirmed, for the first time, that decreased level of miR-212 and elevated expression of FOXA1 were associated with poor clinical features of HCC. [score:3]
A. The expression of miR-212 in HCC tissues was significantly lower than that in matched tumor-adjacent tissues. [score:3]
B. Comparing differences in the expression levels of miR-212 between HCC cell lines with different proliferative potentials and the nontranformed hepatic cell line LO2. [score:3]
Next, we divided patients into four subgroups based on miR-212 and FOXA1 expression levels. [score:3]
Next, Western blot analysis was performed to determine the effect of altering miR-212 expression on FOXA1 abundance in HCC cells. [score:3]
Our data showed that the expression of miR-212 was impaired in HCC tissues. [score:3]
Overexpression of miR-212 decreased the luciferase reporter activity of FOXA1 wt 3′-UTR but not mt 3′-UTR. [score:3]
These results indicate that aberrant expression of miR-212 and FOXA1 is correlated with poor clinical features of HCC patients. [score:3]
To further understand the underlying mechanisms by which miR-212 exerts its biological effects on HCC cells, it is necessary to identify its downstream functional targets. [score:3]
B. Inverse relationship between the expression of miR-212 and FOXA1 was found in HCC specimens. [score:3]
The 3′-UTR sequence of FOXA1 predicted to interact with miR-212 or the mutated sequence within the predicted target sites was synthesized and inserted into the pGL3 control vector (Promega, Madison, WI, USA). [score:3]
These results indicate that miR-212 may be a novel tumor suppressor and may play a critical role in hepatocarcinogenesis. [score:3]
Altering expression of FOXA1 influences the effect of miR-212 on HCC Cells. [score:3]
As measured by qRT-PCR, miR-212 expression vector significantly increased the level of miR-212 in HepG2 cells (P < 0.01, Figure 2A), while the anti-miR-212 vector significantly reduced the expression of miR-212 in Bel-7402 cells (P < 0.01, Figure 2B). [score:3]
In this study, with in vitro and in vivo experiments, we confirmed that miR-212 inhibited cell viability and proliferation, and promoted apoptosis of HCC cells. [score:3]
The expression of miR-212 in HCC tissues was significantly lower than that in matched tumor-adjacent tissues (P < 0.01, Figure 1A). [score:3]
HCC Patients in subgroup I had shortest E. OS and F. DFS, which were divided based on the combination of miR-212 and FOXA1 expression (subgroup I: low miR-212/high FOXA1; subgroup II: low miR-212/low FOXA1; subgroup III: high miR-212/high FOXA1; subgroup IV: high miR-212/low FOXA1). [score:3]
To confirm this prediction, we first examined the relationship between miR-212 and FOXA1 expression in HCC cases. [score:3]
Multivariate Cox regression analysis showed that miR-212 level, FOXA1 expression, tumor size, TNM stage and Edmondenson stage were independent prognostic predictors for both OS and DFS (Table 2). [score:3]
B-E. Altering expression of miR-212 significantly affected the cell viability, proliferation, caspase-3/7 activity, and the percentage of apoptotic cells in HepG2 and Bel-7402 cells. [score:3]
Finally, we confirmed that restoration of FOXA1 expression partly abrogated the functional effect of miR-212 on HCC cell viability, proliferation and apoptosis. [score:3]
Figure 1 A. The expression of miR-212 in HCC tissues was significantly lower than that in matched tumor-adjacent tissues. [score:3]
B-E. Alteration of FOXA1 expression partly abolished the functional effect of miR-212 on cell viability, proliferation, capasase3/7 activity and the percentage of apoptotic cells of HepG2 and Bel-7402 cells. [score:3]
But another study reported that miR-212 promoted pancreatic cancer cell proliferation by inhibiting patched-1 in pancreatic cancer [16]. [score:3]
Moreover, results of our in vitro and in vivo experiments suggest that miR-212 may be a therapeutic target for HCC. [score:3]
The expression level of miR-212 in HCC tissues and cell lines. [score:3]
The critical role of miR-212 and FOXA1 in the tumor growth and their aberrant expressions in HCC tissues promoted us to examine their clinical significance. [score:3]
Taken together, we consider that miR-212 may potentially act as a clinical biomarker, and may also be a therapeutic target, in HCC. [score:3]
Notably, the expression of miR-212 in Bel-7402 and Hep3B cells was higher than that in Huh7 and HepG2 cells (P < 0.01, Figure 1B). [score:3]
In vitro and in vivo studies demonstrated that miR-212 suppressed cell viability and proliferation, and induced apoptosis in HCC cells. [score:3]
Functionally, restoration of FOXA1 expression in HepG2-miR-212 cells partially abrogated the effect of exogenous miR-212, resulting in significant increase of cell viability and proliferation (P < 0.01, respectively, Figure 5B and 5C) and obvious decrease of apoptosis (P < 0.01, respectively, Figure 5D and 5E). [score:3]
An inverse correlation between the expression of miR-212 and FOXA1 protein was observed in HCC tissues. [score:3]
These results confirmed that miR-212 inversely regulated FOXA1 abundance in HCC cells. [score:2]
Furthermore, we confirmed the regulatory effect of miR-212 on FOXA1, AFP and YAP in xenograft tumor tissue (Supplementary Figure 1). [score:2]
MiR-212 inhibits HCC cell proliferation and induces apoptosis in vitro and in vivo. [score:2]
These data indicate that reduced level of miR-212 may be involved in the development of HCC. [score:2]
MiR-212 serves as a tumor suppressor in non-small cell lung cancer (NSCLC) [12] and gastric carcinoma [13]. [score:2]
Reduced expression of miR-212 was observed in all four HCC cell lines as compared with LO2 (P < 0.01, Figure 1B). [score:2]
MiR-212 has been found to inhibit proliferation of gastric cancer by repressing retinoblastoma binding protein-2 [13]. [score:2]
These results demonstrate that FOXA1 is a downstream mediator for the function of miR-212 in HCC. [score:1]
Thus, miR-212 mimics or viral vectors encoding miR-212 may also become the treatment options for HCC in the future. [score:1]
Next, we evaluated the relative expression of miR-212 in a nontransformed hepatic cell line (LO2) and a panel of human HCC cell lines (Bel-7402, Hep3B, Huh7 and HepG2). [score:1]
To further confirm these results in vitro, HepG2 cells that were transfected with miR-212 or control vector were implanted subcutaneously into nude mice. [score:1]
Therefore, it is worth to examine the sensitivity, specificity, and ROC on miR-212 as a diagnostic biomarker for HCC in further study. [score:1]
The percentage of Ki-67 positive cells in tumors arising from HepG2-miR-212 group was significantly lower than that arising from HepG2-miR-control group. [score:1]
The percentage of apoptotic cells in the HepG2-miR-212 group was significantly higher than that in the HepG2-miR-control group. [score:1]
Correlation between the clinicopathologic characteristics and miR-212 and FOXA1 expression in HCC. [score:1]
Therefore, the biological functions of miR-212 are cancer-type specific, partly resulted from the different cellular contexts of various tumors. [score:1]
In this study, we initially evaluated the expression of miR-212 in 40 paired samples of HCC and non-tumor tissues. [score:1]
However, transfection of anti-miR-212 did not lead to obvious alteration of the luciferase activity of FOXA1 containing mt FOXA1 3′-UTR (P < 0.01, Figure 4D). [score:1]
MiR-212, which is located at chromosome 17p13.3 [11], has been shown to be deregulated in various human cancers. [score:1]
Furthermore, we confirmed that miR-212, FOXA1 and the combination of miR-212 and FOXA1 were independent prognostic indicators for OS and DFS of HCC patients. [score:1]
Therefore, the influence of miR-212 on proliferation and apoptosis of malignant cells seems to be elusive and may be dependent on the type of cancer cells. [score:1]
The effect of miR-212 on HCC cell proliferation and apoptosis. [score:1]
Thus, combination of miR-212 and FOXA1 was an independent prognostic predictor for OS and DFS in HCC. [score:1]
The demographic features and clinicopathologic characteristics are presented in Table 1. Then, we divided these enrolled patients into different subgroups based on the expression of miR-212 and FOXA1. [score:1]
When anti-miR-212 was transfected, a significant increase in luciferase activity of wt FOXA1 3′-UTR was observed. [score:1]
Due to its association with AFP, miR-212 can potentially serve as a diagnostic biomarker for HCC. [score:1]
Similarly, silencing of FOXA1 in Bel-7402-anti-miR-212 cells partially abolished the effect of anit-miR-212 on cell viability, proliferation and apoptosis (P < 0.05, respectively, Figure 5B - 5E). [score:1]
Notably, miR-212, FOXA1 and their combination are valuable predictors for the prognosis of HCC patients. [score:1]
Notably, miR-212, FOXA1, and the combination of miR-212 and FOXA1 are independent prognostic factors for OS and DFS of HCC patients. [score:1]
As shown in Table 1, decreased level of miR-212 was associated with high serum AFP level (P = 0.032), large tumor size (P = 0.018) and advanced TNM tumor stage (P = 0.031). [score:1]
However, other studies suggest that miR-212 exhibits oncogenic properties in colorectal cancer [14], prostate cancer [15] and pancreatic cancer [16]. [score:1]
Finally, we found that the 3′-UTR of FOXA1 mRNA contained the complementary sequence of miR-212 (Figure 4A). [score:1]
And the prognostic significance of the combination of miR-212 and FOXA1 was more valuable than miR-212 or FOXA1 alone. [score:1]
The mutant miR-212 binding sites were generated in the complementary site for the seed region of miR-212 (wt, wild type; mt, mutant type). [score:1]
For each cohort, subgroups were divided according to the cutoff values of miR-212 and FOXA1, which was defined as the mean value of the cohort. [score:1]
Clinical significance of miR-212 and FOXA1 in HCC patients. [score:1]
Therefore, miR-212/FOXA1/YAP pathway potentially plays an important role in HCC. [score:1]
The prognostic value of miR-212 and FOXA1 for HCC patients assessed by Kaplen-Merier analysis. [score:1]
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[+] score: 358
To confirm whether XIAP is critical for the function of miR-212 in RCC, we overexpressed XIAP in CAKI-2 cells overexpressing miR-212 and investigated whether restoring XIAP expression could reverse the inhibitory effect of miR-212 on CAKI-2 cells. [score:7]
Therefore, these data indicate that miR-212 inhibits the proliferation, migration and invasion of RCC cells by targeting XIAP protein, and can potentially serve as a promising therapeutic target for RCC. [score:7]
XIAP overexpression reversed the inhibitory effect of miR-212 overexpression on CAKI-2 cells. [score:7]
After confirming the expression and function of miR-212 and XIAP in RCC, we lastly examined whether aberrant expression of miR-212 and its downstream target XIAP could predict the prognosis of RCC patients. [score:7]
The top 8 downregulated (hsa-miR-200c, hsa-miR-212, hsa-miR-29a, hsa-miR-532, hsa-miR-141, hsa-miR-1, hsa-miR-363, hsa-miR-187) and 8 upregulated (hsa-miR-487, hsa-miR-452, hsa-miR-1233, hsa-miR-92a, hsa-miR-106b, hsa-miR-1290, hsa-miR-320, hsa-miR-26a) miRNAs were presented in Figure 1A. [score:7]
The expression level of miR-212 is down-regulated in RCC. [score:6]
In summary, this study finds that miR-212 is down-regulated in RCC and its decreased expression is associated with RCC progression. [score:6]
In this study we demonstrated that overexpression of miR-212 could inhibit the viability, proliferation, migration and invasion of RCC cells while miR-212 knockdown promoted these biological functions of RCC cells. [score:6]
Furthermore, Kaplen-Merier analysis demonstrated that both miR-212 down-regulation and XIAP overexpression predicted the poor prognosis of RCC patients. [score:6]
X-linked inhibitor of apoptosis protein (XIAP) was found to be the direct downstream target of miR-212. [score:6]
Moreover, inhibiting XIAP expression in ACHN cells (P<0.05, Figure 8A) abrogated the promoting effect of miR-212 knockdown on cell viability (P<0.05, Figure 8B), proliferation (P<0.05, Figure 8C), migration (P<0.05, Figure 8D) and invasion (P<0.05, Figure 8E). [score:6]
X-linked inhibitor of apoptosis protein (XIAP), a critical regulator of cell proliferation, apoptosis and motility [17– 19], was predicted to be a potentially downstream target of miR-212. [score:6]
As shown in Figure 7A, XIAP vector significantly increased XIAP expression in in CAKI-2 cells overexpressing miR-212 (P<0.05). [score:5]
To clarify the molecular mechanisms underlying the tumor suppressive roles of miR-212 in RCC, we used the public database to search for the potentially downstream targets of miR-212. [score:5]
On the other hand, miR-212 inhibitor significantly decreased the expression of miR-212 in ACHN cells (P<0.05, Figure 3A). [score:5]
Functionally, overexpressing XIAP reversed the inhibitory effects of miR-212 on cell viability (P<0.05, Figure 7B), proliferation (P<0.05, Figure 7C and 7D), migration (P<0.05, Figure 7F) and invasion (P<0.05, Figure 7F). [score:5]
MiR-212 overexpressing vector, the control vector, miR-212 inhibitor and the negative control were bought from the company of Genecopoeia (Guangzhou, China). [score:5]
Functionally, miR-212 was found to inhibit the growth of hepatocellular carcinoma by targeting FOXA1 [10]. [score:5]
Therefore, these data indicate that miR-212 plays tumor-suppressive role in RCC by inhibiting the proliferation, migration and invasion of RCC cells. [score:5]
These data demonstrate that miR-212 could inhibit the expression of XIAP in RCC cells by interacting with the 3′-UTR of XIAP. [score:5]
Study of gastric cancer also demonstrated that miR-212 inhibited the proliferation of gastric cancer cells by inhibiting [21]. [score:5]
Therefore, miR-212 exerted its tumor suppressive roles in RCC by inhibiting cell viability, proliferation, migration and invasion. [score:5]
Transfection of miR-212 inhibitor significantly decreased the expression of miR-212 in ACHN cells. [score:5]
Taken together, these data demonstrate that miR-212 can inhibit XIAP expression in RCC. [score:5]
ACHN cells in 24-well plates were cultured in OptimMEM reduced serum media (Life Technologies), and were transfected with luciferase reporter construct (the wt or mt 3′-UTR of XIAP) and miR-212 overexpressing vector, miR-212 inhibitor, corresponding control vectors or negative control vectors using Fugene (Promega, Madison, WI, USA). [score:5]
miR-212 overexpression inhibited the in vivo growth of CAKI-2 cells in nude mice. [score:5]
MiR-212 downregulation and XIAP overexpression predict poor prognosis of RCC. [score:5]
In contrast, miR-212 overexpression or knockdown did not have any effect on the luciferase activity of mutated XIAP 3′-UTR (Figure 6B). [score:4]
MiR-212 exerted its tumor suppressive roles in RCC by targeting XIAP. [score:4]
MiR-212 was one of the downregulated miRNAs in RCC tissues. [score:4]
Furthermore, we identify that XIAP protein was the direct downstream target of miR-212. [score:4]
Downregulating miR-212 increased the luciferase activity of wild type XIAP 3′-UTR but not mutated 3′-UTR of XIAP. [score:4]
Figure 3 (A) miR-212 inhibitor was used to knockdown miR-212 in ACHN cells. [score:4]
MiR-212 overexpression significantly inhibited the cell migration and invasion of CAKI-2 cells. [score:4]
In this study, we identified that miR-212 was down-regulated in RCC tissues and cells. [score:4]
The data in Supplementary Figure 1A and 1B showed that miR-212 overexpression increased the Caspase3/7 activity while its knockdown decreased the Caspase3/7 activity (P<0.05). [score:4]
MiR-212 overexpression inhibited the cell viability, proliferation, migration and invasion of CAKI-2 cells. [score:4]
MiR-212 overexpression significantly inhibited the cell viability of CAKI-2 cells. [score:4]
Overexpression of miR-212 significantly decreased while miR-212 knockdown significantly increased the luciferase activity of wild type XIAP 3′-UTR (P<0.05, Figure 6B). [score:4]
RCC patients with low expression level of miR-212 had significantly decreased rate of Overall survival (OS) (A) and Recurrent-free survival (RFS) (B). [score:3]
Transfection of miR-212 mimic significantly increased the expression of miR-212 in CAKI-2 cells. [score:3]
Figure 7 (A) The XIAP vector significantly increased the mRNA and protein level of XIAP in CAKI-2 overexpressing miR-212. [score:3]
Decreased expression level of miR-212 was correlated with poor prognosis of RCC patients. [score:3]
These data indicate that XIAP is not only a downstream target of miR-212, but also a functional mediator of miR-212 in RCC. [score:3]
Previous stduies showed FOXA1, HBEGF, MECP2 and PED were the downstream targets of miR-212 in different types of cells. [score:3]
On the other hand, miR-212 was also found to be overexpressed and play oncogenic roles in pancreatic cancer [15, 16]. [score:3]
The expression of XIAP in RCC tissues was negatively correlated with miR-212 level. [score:3]
In vivo studies also confirmed that miR-212 inhibited the growth of RCC cells in nude mice. [score:3]
Furthermore, and western blot confirmed that miR-212 overexpression decreased the mRNA (P<0.05, Figure 5C) and protein (P<0.05, Figure 5D) level of XIAP in CAKI-2 cells. [score:3]
XIAP mediates the tumor suppressive functions of miR-212 in RCC. [score:3]
XIAP knockdown abrogated the promoting effect of miR-212 knockdown on ACHN cells. [score:3]
RCC patients with high expression level of miR-212 had significantly decreased rate of OS (C) and RFS (D). [score:3]
However, the expression and function of miR-212 in RCC remain unknown. [score:3]
The expression of miR-212 was significantly decreased in RCC tissues of TNM I stage. [score:3]
Furthermore, the expression level of miR-212 in RCC tissues at stage II-IV was significantly decreased (P<0.05, Figure 1D). [score:3]
MiR-212 overexpression significantly inhibited the cell proliferation of CAKI-2 cells, as suggested by BrdU assay and 3D culture. [score:3]
Ki67 staining and Tunel staining confirmed that miR-212 overexpression significantly decreased the proliferation (P<0.05, Figure 4B) and decreased the apoptosis (P<0.05, Figure 4B) of CAKI-2 cells in nude mice. [score:3]
IAP expression is negatively correlated with miR-212 level in RCC tissues. [score:3]
These data demonstrate that miR-212 is a tumor suppressive microRNA in RCC. [score:3]
The expression of miR-212 was significantly decreased in RCC tissues. [score:3]
further confirmed that the expression of miR-212 was significantly decreased in RCC tissues. [score:3]
Figure 4MiR-212 inhibited the in vivo growth of RCC cell in nude mice (A) CAKI-2 control cells and CAKI cell overexpressing miR-212 were subcutaneous injected into nude mice to investigate the effect of miR-212 on in vivo growth of RCC cells. [score:3]
XIAP is the downstream target of miR-212 in RCC. [score:3]
Overexpression of miR-212 significantly decreased the cell viability of CAKI-2 cells (P<0.05, Figure 2B). [score:3]
In this study,, western blot and luciferase activity assay demonstrated that XIAP was the direct downstream target of miR-212 in RCC. [score:3]
To clarify the detailed mechanisms by which miR-212 exerts tumor suppressive effects in RCC cells, we further investigated the downstream target of miR-212. [score:3]
However, study of pancreatic cancer cells found that miR-212 promoted cell proliferation by targeting patched-1 [16]. [score:3]
CAKI-2 cells transfected with miR-212 overexpressing vector or control vectors were suspended in 100 uL PBS and were injected subcutaneously into the flank of nude mouse. [score:3]
Transfection of miR-212 overexpressing vector into CAKI-2 cells significantly increased miR-212 level in CAKI-2 cells (P<0.05, Figure 2A). [score:3]
The expression of miR-212 was significantly decreased in RCC tissues of T1 stage. [score:3]
The mean expression level of miR-212 and XIAP was defined as cutoff value to divide RCC patients into: miR-212 low group and high group, and, XIAP low group and high group. [score:3]
XIAP was the downstream target of miR-212 in RCC. [score:3]
Figure 2 (A) miR-212 mimic was used to overexpress miR-212 in CAKI-2 cells. [score:3]
As shown in Figure 9A and 9B, decreased expression of miR-212 was correlated with decreased rate of overall survival (OS) (P<0.05) and recurrent-free survival (RFS) (P<0.05). [score:3]
In vitro and in vivo studies confirm that miR-212 inhibit the proliferation, migration and invasion of RCC cells. [score:3]
MiR-212 inhibited the in vivo growth of RCC cell in nude mice. [score:2]
MiR-212 level was negatively correlated with XIAP expression in RCC tissues. [score:2]
MiR-212 inhibited the proliferation, migration and invasion of RCC cells. [score:2]
BrdU and 3D culture demonstrated that compared with control vector, miR-212 overexpressing vector significantly decreased the proliferative ability of CAKI-2 cells (P<0.05, Figure 2C and 2D). [score:2]
MiR-212 expression was decreased in RCC. [score:2]
Western blot further demonstrated that in RCC tissues with high miR-212 level, the expression of XIAP was significantly decreased, compared with the tissues of low miR-212 level (P<0.05, Figure 6C). [score:2]
Furthermore, Transwell assay confirmed that forced expression of miR-212 significantly reduced the migration (P<0.05, Figure 2E) and invasion (P<0.05, Figure 2F) of CAKI-2 cells. [score:2]
Compared with HK-2 cells, the expression of miR-212 was significantly decreased in RCC cell lines (ACHN, 786-O, SN12PM6, OS-RC-2 and CAKI-2). [score:2]
Figure 8 (A) The XIAP shRNA significantly decreased the mRNA and protein level of XIAP in ACHN cells with miR-212 knockdown. [score:2]
MiR-212 level was negatively correlated with XIAP expression level in RCC tissues. [score:2]
Knockdown of miR-212 resulted in increased cell viability (P<0.05, Figure 3B), proliferation (P<0.05, Figure 3C and 3D), migration (P<0.05, Figure 3E) and invasion (P<0.05, Figure 3F) of ACHN cells. [score:2]
Compared with CAKI-2 cells transfected with control vector, CAKI-2 cells overexpressing miR-212 showed significantly decreased in vivo growth ability (P<0.05, Figure 4A). [score:2]
MiR-212 inhibits the proliferation, migration and invasion of RCC cells. [score:2]
To further confirm the regulatory effect of miR-212 on XIAP, we measured the expression level of XIAP in RCC tissues. [score:2]
Lastly, we evaluated the expression level of miR-212 in RCC cell lines. [score:1]
Lastly, miR-212 and XIAP are prognostic predictors for RCC patients. [score:1]
In RCC tissues of advanced T stage and TNM stage, the level of miR-212 was significantly decreased. [score:1]
GAPDH and U6 were used as the internal control for XIAP and miR-212, respectively. [score:1]
Taken together, these data indicate miR-212 is significantly decreased in RCC tissues and cells. [score:1]
More importantly, XIAP was found to mediate the functional influence of miR-212 on cell viability, proliferation, migration and invasion. [score:1]
Mutated XIAP 3′-UTR was generated in the complementary site for the seed region of miR-212. [score:1]
To investigate the functional role of miR-212 in RCC, we overexpressed miR-212 in CAKI-2 cells. [score:1]
Addtionally, we examined the effect of miR-212 on the Caspase3/7 activity on RCC cells. [score:1]
Among these miRNAs, miR-212 was one of the top downregualted miRNAs in RCC. [score:1]
MiR-212 knockdown significantly promoted the cell migration and invasion of ACHN cells. [score:1]
Correlation analysis for XIAP and miR-212 showed that the level of miR-212 was negatively correlated with the XIAP level in RCC tissues (P<0.05, Figure 6B). [score:1]
MiR-212 knockdown promoted the cell viability, proliferation, migration and invasion of ACHN cells. [score:1]
MiR-212 knockdown significantly promoted the cell viability of ACHN cells. [score:1]
These indicate that miR-212 and XIAP can both serve as prognosis predictor for RCC patients. [score:1]
These indicate that miR-212 and XIAP are promising prognostic predictors for RCC patients. [score:1]
XIAP level was significantly decreased in RCC tissues with high level of miR-212 [*], P<0.05 by t test and Spearman's correlation analysis. [score:1]
MiR-212 knockdown increased the mRNA (P<0.05, Figure 5E) and protein (P<0.05, Figure 5F) level of XIAP in CAKI-2 cells. [score:1]
Furthermore, we demonstrated that miR-212 was significantly decreased in RCC cell lines. [score:1]
The prognostic value of miR-212 and XIAP for RCC patients assessed. [score:1]
As shown in Figure 5A, XIAP 3′-UTR contained the complementary sequences for miR-212 binding. [score:1]
Among numerous miRNAs, miR-212 was one of the significantly downregualted miRNAs in RCC tissues. [score:1]
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[+] score: 318
Overexpression of hsa-miR-212 suppressed RBP2 expression, with inhibited cell proliferation and induced cellular senescence, which coincided with upregulated CDKIs; with low hsa-miR-212 expression, CDKIs were downregulated in HCC tissue. [score:17]
In conclusion, our findings suggest that overexpressed RBP2 in HCC resulted from downregulated hsa-miR-212 expression and that overexpressed RBP2 could promote cell proliferation and suppress cell senescence by downregulating p16 [ink4a], p21 [CIP2] and p27 [kip1]. [score:15]
Figure S1 RBP2 expression was inhibited with transfection of RBP2 siRNA or enhanced with transfection of RBP2 overexpression plasmid in HCC cell lines and RBP2 was negatively regulated by hsa-miR-212 (A–B) RT-PCR analysis of the mRNA expression of RBP2 with transfection of RBP2 siRNA or RBP2 overexpression plasmid. [score:12]
RBP2 expression was induced with hsa-miR-212 inhibition in HCC cell lines, and reduced p16 [ink4a] and p27 [kip1] expression was confirmed by qRT-PCR method in HCC with downregulated hsa-miR-212 expression. [score:12]
0069784.g005 Figure 5RBP2 expression was induced with hsa-miR-212 inhibition in HCC cell lines, and reduced p16 [ink4a] and p27 [kip1] expression was confirmed by qRT-PCR method in HCC with downregulated hsa-miR-212 expression. [score:12]
Here, we found that RBP2 is a direct target of hsa-miR-212, and overexpressed RBP2 in HCC tissues may result from downregulated hsa-miR-212 expression. [score:11]
So, the low expression of hsa-miR-212 in HCC may result in overexpression of RBP2 and downregulation of RBP2 targets such as CDKIs, accompanied by cell proliferation and blocking cellular senescence in HCC, which contributes to its pathogenesis. [score:10]
Conversely, inhibition of hsa-miR-212 expression upregulated RBP2 expression. [score:10]
Furthermore, the expression of p16 [ink4a] and p27 [kip1] was downregulated in HCC tissues with inhibited hsa-miR-212 expression (both P<0.001; Figure 5F ). [score:10]
Inhibition of hsa-miR-212 expression upregulated RBP2 expression. [score:10]
As well, downregulation of hsa-miR-212 may be due to hypermethylation of DNA in the hsa-miR-212 promoter because downregulation of hsa-miR-212 expression is through DNA hypermethylation in human gastric cancer [40]. [score:9]
Induced epigenetic molecules could also regulate the expression of miRNAs [42]– [44], but we found no evidence of induced RBP2 affecting hsa-miR-212 expression because siRNA knockdown of RBP2 did not change the expression of hsa-miR-212 (Figure S1E). [score:9]
Effect of hsa-miR-212 inhibition on (A) qRT-PCR analysis of mRNA expression of Hsa-miR-212 and RBP2, (B) western blot analysis of protein expression of RBP2, and (C) qRT-PCR analysis of mRNA expression of p16 [ink4a] and p27 [kip1]. [score:9]
Therefore, low hsa-miR-212 expression resulted in overexpressed RBP2, which contributed to downregulation of p16 [ink4a] and p27 [kip1], thus confirming the hsa-miR-212–RBP2–CDKI pathway involved in HCC. [score:8]
Also, downregulated hsa-miR-212 expression may not be the only mechanism leading to the overexpression of RBP2. [score:8]
With hsa-miR-212 overexpression in HepG-2 and SMMC-7721 cells, hsa-miR-212 expression was significantly increased, which confirmed the success of hsa-miR-212 overexpression (Figure 4A ). [score:7]
RBP2 expression was suppressed with hsa-miR-212 overexpression. [score:7]
RBP2 inhibition and hsa-miR-212 overexpression may lead to cell proliferation arrest and cellular senescence by depressing cyclin -dependent kinase inhibitors (CDKIs; p16 [ink4a], p21 [CIP2] and p27 [kip1]). [score:7]
To ascertain whether hsa-miR-212 directly regulated the expression of RBP2, use of an RBP2 3′-UTR reporter vector significantly decreased luciferase activity with hsa-miR-212 overexpression in SMMC-7721 cells. [score:7]
To further confirm that RBP2 was negatively regulated by hsa-miR-212, transfection of hsa-miR-212 inhibitor plasmid in the 2 cell lines decreased the expression of hsa-miR-212 (Figure 5A ) and increased that of RBP2 (Figure 5A and B ; Figure S1D). [score:6]
Downregulation of hsa-miR-212 increasing the expression of HB-EGF may be involved in cetuximab resistance in head and neck squamous cell carcinoma [20]. [score:6]
To confirm that RBP2 was negatively regulated by hsa-miR-212 and could affect cell proliferation, HepG-2 cells with hsa-miR-212 overexpression showed decreased RBP2 expression, with decreased cell proliferation (Figure 5E, left). [score:6]
We found that Hsa-miR-212 directly binds to the 3′ UTR of RBP2 and suppressed its expression. [score:6]
RBP2 expression was markedly repressed with hsa-miR-212 overexpression (Figure 4B and C ; Figure S1C). [score:5]
Accordingly, the expression of p16 [ink4a] and p27 [kip1] was decreased with hsa-miR-212 inhibition (Figure 5C ). [score:5]
We found that depletion of one miRNA, hsa-miR-212, antagonized the suppression of RBP2, which led to RBP2 overexpression in HCC, but further investigation is needed to elucidate the reason for the overexpressed RBP2 in HCC. [score:5]
RBP2 is overexpressed and hsa-miR-212 underexpressed in human HCC. [score:5]
0069784.g004 Figure 4(A) qRT-PCR analysis of Hsa-miR-212 mRNA expression in cancer cells with hsa-miR-212 overexpression. [score:5]
Low expression of hsa-miR-212 and overexpression of RBP2 may be prognostic markers for HCC. [score:5]
SMMC-7721 cells with hsa-miR-212 inhibitor showed increased RBP2 expression, with enhanced cell proliferation (Figure 5E, right). [score:5]
RBP2 was overexpressed and hsa-miR-212 underexpressed in human hepatic cancer tissues. [score:5]
As well, RBP2 and hsa-miR-212 expression may be a therapeutic target for HCC. [score:5]
However, other mechanisms may lead to the suppression of hsa-miR-212 expression in HCC. [score:5]
Hsa-miR-212, the predicted miRNA that could bind to the 3′ UTR of RBP2 (Figure 1D ), may regulate its expression in these clinical samples. [score:4]
Thus, RBP2 was a direct target of hsa-miR-212. [score:4]
We found that RBP2 is overexpressed in HCC and negatively regulated by hsa-miR-212. [score:4]
Recently, miR-212 expression was found to be deregulated in lung cancer [41]. [score:4]
However, the mechanism by which hsa-miR-212 is downregulated in HCC is not known. [score:4]
RBP2 is overexpressed in HCC and negatively regulated by hsa-miR-212. [score:4]
RBP2 and hsa-miR-212 may be biomarkers for diagnosis of HCC and therapeutic targets in its treatment. [score:3]
Accordingly, cell proliferation was repressed and cell senescence induced with hsa-miR-212 overexpression (Figure 4E and F ). [score:3]
The expression of RBP2 was stronger in cancerous than non-cancerous tissues, but that of its binding microRNA, Homo sapiens miR-212 (hsa-miR-212), showed an opposite pattern. [score:3]
We found that RBP2 is a target of hsa-miR-212, and hsa-miR-212 could bind with 2 regions of the 3′ UTR of RBP2 (Figure 1D ). [score:3]
The expression of RBP2 was stronger in cancerous than non-cancerous human tissues, but that of its binding miRNA, hsa-miR-212, was reversed. [score:3]
Overexpression of hsa-miR-212 had a similar effect. [score:3]
Hsa-miR-212 level was significantly lower in HCC than normal tissue (P<0.001; Figure 1E ), which suggested a negative regulation between RBP2 and hsa-miR-212 in HCC. [score:2]
The hsa-miR-212–RBP2–CDKI pathway in HCC may contribute to its initiation and development. [score:2]
However, co-transfection of hsa-miR-212 with the 2 mutants of the RBP2 3′ UTR reporter vector (mutation of the 2 binding sites of RBP2, Table 2 ) reversed the luciferase activity (Figure 5D ). [score:2]
RBP2 was Negatively Regulated by hsa-miR-212. [score:2]
The hsa-miR-212–RBP2–CDKI pathway may be important in the pathogenesis of HCC. [score:1]
Homo sapiens miRNA-212 (hsa-miR-212) has 2 sites binding in the 3′ UTR of RBP2. [score:1]
Luciferase reporter assay detected the direct binding of hsa-miR-212 to the RBP2 3′ UTR. [score:1]
RBP2 and miR212 levels were negatively correlated (R [2] = 0.7941, Figure 1F ). [score:1]
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Consistently, inhibition of the miRNA cluster by transfection of antisense (as-) into the TCDD- or DIM -treated breast cancer cells mitigated the agonists’ inhibitory effects on invasion of MDA-MB-231 and T47D (Fig.   3c), suggesting a direct inhibitory role of miR-212/132 on motility of MDA-MB-231 and T47D cells. [score:8]
Interestingly, miR-212/132 over -expression showed direct anti-migration, anti-expansion and anti-invasion properties, and an inhibition of the miRNA cluster mitigated the anti-invasive properties of TCDD and DIM. [score:6]
The suppressive effects of TCDD and DIM on metastasis of breast cancer cells is concomitant with higher miR-212/132 expression. [score:5]
The current results, for the first time, demonstrated that toxic and non-toxic Ahr agonists suppressed breast cancer metastasis through triggering the transcription of SOX4 -targeting miR-212/132 cluster. [score:5]
In the current study, over -expression of miR-212/132 showed anti-invasive properties, and inhibition of Ahr agonist -induced miRNA cluster abrogated the agonists’ anti-invasive properties in MDA-MB-231 and T47D. [score:5]
c Inhibition of miR-212/132 cluster by antisense partially blocked the inhibitory effects of TCDD and DIM on invasion of MDA-MB-231 and T47D cells. [score:5]
An application of miRNA target scan algorithm, i. e., MiRaNda [32], predicted that SOX4 is a candidate target gene of the miR-212/132 cluster (Fig.   4e). [score:5]
Agonist-activated Ahr regulates miR-212/132 expression in breast cancer cells. [score:4]
b and d * P < 0.05, significantly different from DMSO -treated control or Ahr agonist- and siAhr-treatments To investigate whether Ahr was directly involved in miR-212/132 expression, first, Ahr was inhibited by RNA interference. [score:4]
b and d * P < 0.05, significantly different from DMSO -treated control or Ahr agonist- and siAhr-treatmentsTo investigate whether Ahr was directly involved in miR-212/132 expression, first, Ahr was inhibited by RNA interference. [score:4]
Activation of Ahr by TCDD and DIM decreased the luciferase activities significantly, and these effects were reversed by co-transfection with as-miR-132 (Fig.   4c) and as-miR-212 (Fig.   4d), suggesting a regulatory role of the miRNA cluster on SOX4 gene expression. [score:4]
Knockdown of Ahr in Ahr agonists -treated cells significantly inhibited the luciferase activity driven by miR-212/132 promoter (Fig.   2d). [score:4]
TCDD and DIM down-regulate SOX4 in breast cancer cells by triggering Ahr-miR-212/132 axis. [score:4]
These results suggested that the agonist-activated Ahr was involved in up-regulation of miR-212/132 in both breast cancer cell lines. [score:4]
It was further shown that miR-212/132 cluster is a metastasis suppressor in breast cancer cells. [score:3]
Collectively, the results demonstrated for the first time that Ahr directly regulated miR-212/132 transcription by functional binding on miR-212/132 promoter. [score:3]
These results suggest a new mechanism through which miR-212/132 mediate the anti-metastatic properties of TCDD and DIM by targeting the pro-metastatic factor SOX4. [score:3]
As shown in Fig.   4f, over -expression of miR-212/132 significantly decreased the luciferase activity. [score:3]
a TCDD (1–25 nmol/L) and DIM (10–50 μmol/L) induced miR-212/132 cluster in MDA-MB-231 and T47D cells, miRNA expression was quantified by real-time PCR. [score:3]
Fig. 4TCDD and DIM suppress the pro-metastatic factor SOX4 by inducing the miR-212/132 cluster. [score:3]
Notably, the effects of Ahr agonists on SOX4 were repealed by Ahr knockdown and partially reversed by miR-212/132 antisense in Ahr agonist -treated cells, suggesting an involvement of other molecules, i. e., miRNAs, in the regulatory role of Ahr agonists on SOX4. [score:3]
Efficiency of miR-212/132 inhibition by antisense was confirmed by real-time-PCR as shown in Fig.   3d. [score:3]
These results identified SOX4 as a new target gene of the miR-212/132 cluster in MDA-MB-231 and T47D cells. [score:3]
c and d Co-transfection of 3′UTR-SOX4-luc and miRNA antisense, as-miR-132 or as-miR-212, mitigated the inhibitory effects of TCDD and DIM on the luciferase activity in MDA-MB-231 and T47D. [score:3]
c TCDD and DIM induced the miR-212/132 expression in pulmonary nodules of MDA-MB-231- or T47D -injected mice. [score:3]
A direct regulatory role of Ahr on the miR-212/132 gene by association with XRE boxes was tested by, and confirmed by luciferase activity. [score:3]
Inhibition of miR-212/132 in Ahr-agonist treated cells mitigated the anti-invasive effects of the agonists, and transfection with mimics showed supporting results, suggesting that miR-212/132 cluster mediated, at least partially, the anti-invasive effects of TCDD and DIM. [score:3]
Taken together, the findings provide the first evidences of the synergistic anti-metastatic properties of miR-212/132 cluster through suppression of SOX4. [score:3]
TCDD, and to a lesser extent DIM, significantly induced the expression of miR-212/132 cluster in the isolated nodules of MDA-MB-231- or T47D -injected mice (Fig.   5c). [score:3]
Fig. 5TCDD and DIM suppress metastasis of breast cancer cells to the lungs and induce miR-212/132 in vivo. [score:3]
The expression of miR-212/132 cluster and coding genes were examined by real-time PCR, and the protein levels were detected by western blot. [score:3]
Effects of TCDD and DIM and two additional Ahr agonists on miR-212/132 expression in breast cancer cells. [score:3]
SOX4 is a new target gene of miR-212/132 cluster in breast cancer cells. [score:3]
a Over -expression of the miR-212/132 cluster by mimics suppressed the migration of MDA-MB-231 and expansion of T47D cells in wound healing assay compared with siNS -transfected control. [score:3]
e SOX4 is a potential target gene of the miR-212/132 cluster; complementary binding site of miR-212/132 on the SOX4 3′UTR. [score:3]
MiR-212/132 has a direct inhibitory role on motility of breast cancer cells. [score:3]
To support these findings, two more Ahr-specific agonists were used to examine their effects on the miR-212/132 cluster expression. [score:3]
Over -expression of miR-132 and miR-212 showed inhibitory effects on migration of MDA-MB-231 and expansion of T47D cells in wound healing assay, and invasion in Boyden chamber in both cell lines compared with siNS -transfected controls (Fig.   3a and b). [score:3]
To further test a direct regulatory role of Ahr, 1 kb of miR-212/132 promoter was analyzed for the xenobiotic responsive elements (XRE) using transcription factor prediction software. [score:3]
Together, these results confirmed for the first time that Ahr directly regulated the transcription of miR-212/132 gene. [score:3]
Over -expression of miR-212/132 in both cell lines decreased SOX4 mRNA (Additional file 1: Figure S5A and B). [score:3]
A reciprocal correlation was identified between Ahr agonists -induced miR-212/132 and the pro-metastatic SRY-related HMG-box4 (SOX4), and a new specific binding sites for miR-212/132 were identified on the untranslated region (3′UTR) of SOX4. [score:3]
f Co-transfection of 3′UTR-SOX4-luc and miRNA mimics, miR-132 or miR-212, suppressed the luciferase activity in MDA-MB-231 and T47D. [score:3]
Potential binding sites of miR-212/132 cluster (HGNC:31589/HGNC:31516) on the 3′UTR of SOX4 (HGNC:11200) were queried by the miRNA target prediction software microRNA. [score:3]
d siAhr suppressed the luciferase activity of miR-212/132 promoter reporter. [score:3]
Taken together, the results identified SOX4 as a new target gene of the miR-212/132 cluster in human breast cancer cells. [score:3]
The binding specificity of miR-212/132 cluster on the SOX4 3′UTR was examined by mutation in the sequence on which miR-212/132 seed sequence bind (from GACTGTT to GAGACGG). [score:2]
b Mimics of the miR-212/132 cluster suppressed the invasion of MDA-MB-231 and T47D cells in the Boyden chamber assay. [score:2]
To study whether the miR-212/132 cluster has a direct role on motility of breast cancer cells, the cluster mimics were transfected separately into MDA-MB-231 and T47D cells. [score:2]
b siAhr blocked the 10 nmol/L TCDD- and 25 μmol/L DIM -induced miR-212/132 expression in MDA-MB-231 and T47D cells compared with the siNS -transfected control. [score:2]
MiR-212 and miR-132 are tandem miRNAs at the same location on chromosome 17 in humans, called miR-212/132 cluster, and they share the same seed sequence and the transcriptional regulatory elements. [score:2]
The miR-212/132 cluster was transcriptionally activated in MDA-MB-231 and T47D cells by TCDD and DIM, and this activation was regulated by Ahr. [score:2]
Both TCDD and DIM reduced the luciferase activity of the 3′UTR-SOX4 construct that contains the predicted binding sites for the miR-212/132 cluster, and mutation in these sites restored the luciferase activity. [score:2]
Analysis of the regulatory elements of the miR-212/132 gene using online software, i. e., Promo V3.0.2 [31], revealed the presence of two XRE boxes (GCGTG) located within 1 kb relative to the transcription site. [score:2]
Analysis of the regulatory elements of the miR-212/132 gene was performed using transcription factor prediction software [http://alggen. [score:2]
Chinen I, Nakahama T, Kimura A, Nguyen NT, Takemori H, Kumagai A, et al. The aryl hydrocarbon receptor/microRNA-212/132 axis in T cells regulates IL-10 production to maintain intestinal homeostasis. [score:2]
For example, miR-212/132 cluster is involved in mammary gland development [9, 10], neuronal differentiation and cognitive processes [11– 13], cardiac hypertrophy and cardiomyocyte autophagy [14], autoimmune inflammation [15], vasodilatory function and angiogenic responses [16]. [score:2]
Thus, the effects of TCDD and DIM on miR-212/132 expression and metastatic features in human breast cancer cells were investigated. [score:1]
Further in vivo studies demonstrated that the Ahr-miR-212/132-SOX4 module was induced by Ahr activation. [score:1]
Taken together, the results not only provide a new miRNA -based mechanism to understand the anti-metastatic properties of Ahr agonists, but also provide the first evidence of the synergistic anti-metastatic properties of the members of miR-212/132 cluster in human breast cancer cells, opening intriguing possibilities of using this miRNA cluster as an innovative therapeutic strategy for breast cancer. [score:1]
These effects were abrogated when the 3′UTR-SOX4-luc was replaced with a reporter contains a mutated sequence where miR-212/132 seed sequence binds (Fig.   4g). [score:1]
The role of miR-212/132 cluster on migration of MDA-MB-231, expansion of T47D and invasion of breast cancer cells were examined by the transfection of miRNA mimics, miR-132 and miR-212, or antisense, as-miR-132, as-miR-212. [score:1]
a– d * P < 0.05, significantly different from Veh -treated controlTo test whether Ahr agonists induce miR-212/132-SOX4 module in vivo, miRNA cluster and SOX4 mRNA were quantified in the pulmonary nodules. [score:1]
The 3′UTR-SOX4-luc construct (SwitchGear Genomics, Menlo Park, CA) was co -transfected with miR-212/132 mimics or antisense (Ambion) at 250 nmol/L as previously described [45]. [score:1]
To examine the hypothesis of Ahr-miR-212/132 axis in breast cancer cells, the expression of miR-212/132 cluster was measured by real-time PCR. [score:1]
The Ahr physically bound to the XRE-2 located at 830 bp from miR-212/132 transcription site (Fig.   2c). [score:1]
Fig. 2TCDD and DIM induce miR-212/132 cluster in breast cancer cells in an Ahr -dependent fashion. [score:1]
Finally, luciferase activity was quantified in breast cancer cells co -transfected with miR-212/132 promoter reporter and siAhr. [score:1]
a– d * P < 0.05, significantly different from Veh -treated control To test whether Ahr agonists induce miR-212/132-SOX4 module in vivo, miRNA cluster and SOX4 mRNA were quantified in the pulmonary nodules. [score:1]
MiR-212 and miR-132 are tandem miRNAs located in an intergenic region on chromosome 17 in humans, and they share the same seed sequence AACAGUCU. [score:1]
In recent studies, we found that TCDD and 6-formylindolo[3,2-b]carbazole (FICZ) induced the highly conserved miR-212/132 cluster in the murine cellular immune compartment [15, 30]. [score:1]
Effects of miR-212/132 mimics on mRNA level of SOX4. [score:1]
Recently, we demonstrated that agonist-activated Ahr induced a highly conserved miRNA cluster, named miR-212/132, in murine cellular immune compartment. [score:1]
The siAhr and siNS control (Ambion, Austin, TX) were co -transfected with the miR-212/132 promoter reporter at the final concentration of 75 nmol/L. [score:1]
c analysis of Ahr binding activity on XRE box on upstream sequence of miR-212/132 gene. [score:1]
miR-212/132 Aryl hydrocarbon receptor Breast cancer Metastasis Breast cancer is the most common cause of cancer -associated deaths amongst women in developed and developing countries [1]. [score:1]
For endogenous controls, GAPDH was used for Ahr, CYP1A1 and SOX4, and RNU6B was used for miR-212/132. [score:1]
d Efficiency of miR-212/132 knockdown by antisense compared with siNS was confirmed by real-time PCR. [score:1]
The MDA-MB-231 and T47D cells were transfected with 3′UTR-SOX4-luc construct, which contains the candidate binding sites for miR-212/132 cluster (MiRaNda v. 21) [32]. [score:1]
Besides, biological effects of Ahr-miR-212/132 axis were examined in vitro by cell migration, expansion and invasion, and examined in vivo by orthotopic mo del of spontaneous metastasis. [score:1]
Consistent with the in vitro results, TCDD induced a reciprocal correlation between miR-212/132 and SOX4 in vivo, which may explain, at least partially, the anti-metastatic properties. [score:1]
Therefore, it was hypothesized here that the miR-212/132 cluster may be induced in human breast cancer cells by Ahr agonists, and may contribute to their anti-metastatic properties. [score:1]
In previous studies, we demonstrated that activation of Ahr by TCDD and FICZ induced the highly conserved miR-212/132 cluster in murine cellular immune compartment, and supporting results were obtained in Ahr [−/−] mice [15, 30, 45]. [score:1]
Also, co-transfection of the 3′UTR-SOX4-luc and miR-212/132 mimics or miRNA mimics alone showed supporting results. [score:1]
Also, current study suggest a new miRNA -based mechanism elucidating the anti-metastatic properties of Ahr agonists, suggesting possibility of using miR-212/132 to control metastasis in breast cancer patients. [score:1]
Therefore, it was predicted in the current study that Ahr agonists induce miR-212/132 in human breast cancer cell lines, and these miRNAs may contribute to the anti-tumor properties of these agonists. [score:1]
To examine this prediction, MDA-MB-231 and T47D cells were first transfected with miR-212/132 mimics. [score:1]
g MiRNA mimics did not decrease the luciferase activity when co -transfected with 3′UTR-SOX4-luc that contains mutated binding sites for miR-212/132. [score:1]
The effects of Ahr agonists on Ahr-miR-212/132-SOX4 module in vivo were tested using an established orthotopic mo del of tumor growth and spontaneous metastasis. [score:1]
illustrated in Fig.   2b show that siAhr blocked the Ahr agonist -induced miR-212/132 cluster. [score:1]
The cells were also co -transfected with 3′UTR-SOX4-luc construct and miR-212/132 mimics. [score:1]
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Other miRNAs from this paper: hsa-mir-1-2, hsa-mir-122, hsa-mir-132, hsa-mir-206, hsa-mir-1-1
When miR-212-3P and miR-132-3P determined as discussion objects, we firstly analyze the expression of miRNA and its target genes across human tissues, the result provide a sound basis for its involvement in neurological diseases such as epilepsy that miR-132/212 presents brain tissue-specific and elevated expression, there are far more similar example like miR-1/133a and miR-206/133b cluster, known as myomiRs, that suppress key genes in muscle development [15]; the liver-specific miRNA-122* and miR-122 participates extensively in human hepatocellular carcinoma [38, 39]. [score:12]
Then, a great deal of studies have demonstrated that marked increase in transcription from the miR-132/212 locus can be caused by neuronal stimulation, and the expression of miR-132 and miR-212 is necessary for the proper development, maturation, morphogenesis and function of neurons and whose dysregulation has more to do with a large amount of neurodegenerative disorders, such as tauopathies, schizophrenia, Alzheimer's disease, Huntington's disease, autism and the theme of this article, epilepsy. [score:9]
In humans, the miR-212/132 gene cluster exhibit similar mature sequences and share identical 8 base identical seed sequences, by which they may therefore target the same mRNAs and then involved in translational inhibition of these target genes [7]. [score:9]
Previous study coming from our and others have found miR-132 presented tumor-promoting but miR-212 served as tumor-suppressing feature in stomach adenocarcinoma (STAD) [27, 28], in here, the genes, i. e., SIRT1 and MECP2 with such similar reverse feature were shown to be down-regulated and up-regulated in STAD [29, 30], have conspicuously negative connection with miR-132-3p and miR-212-3p in STAD, which partially confirms the fact that both miRs have reverse functions in some tumors. [score:9]
TargetScanhuman7.1 was used to predicts biological targets of miR-212-3P/miR-132-3P, all remaining gene (refer to the gene that have ruled out the experimentally validated target gene from all predicted target gene) performed enrichment analysis of gene-GO term, bio-pathways as described above. [score:9]
Given all that, survival analysis sourced from TCGA data was performed and the result showed that miR-132-3p and miR-212-3p were presented to be up-regulated or down-regulated in different cancer types, and Kaplan-Meier analysis curves demonstrated that aberrantly expression of both miRs was conspicuously associated with poor overall survival (Figure 4A). [score:9]
So we want to make clear whether the expression of miR-132-3p and miR-212-3p have got relatively nerve tissue specifity, the data coming from the Human miRNA tissue atlas showed that miR-132-3p and miR-212-3p have a high concordance of brain tissue-specific expression in human, which indicated these miRs play a pivotal role in brain tissue development and impaired expression of them may result in disorders of the nervous system. [score:8]
To achieve a more comprehensive analysis of target gene, the same analysis was carried on remaining predicted targets, Axon guidance ranked first in these genes, previous study have found hippocampal axon guidance can be regulated by nor-1 and involve in seizure susceptibility [44], and mTOR signaling pathway can sever as a new therapeutic strategy in epilepsy and epileptogenesis, all which absented in validated target genes may be provide a valuable reference and guide for future study on miR-212/132in epilepsy. [score:8]
Although their role in neuronal functions is the most studied, more evidences point towards an involvement of these miRNAs in human cancer have been found such as miR-212 may improve the current prognostic risk stratification of mixed acute myeloid leukemia [9], epigenetic regulation of miR-212 expression in lung cancer [10] and down-regulation of microRNA-132 is associated with poor prognosis of colorectal cancer [11]. [score:7]
Firstly, we want to know whether the 570(2 gens in Original article significantly associated epilepsy were include) DEGs can directly target by miR-132-3p and miR-212-3p, the intersections between DEGs and target genes derived from different source were calculated, Surprisingly and fascinating, venn diagram shown that 31.1%(177/570) DEGs may be target by both miRs and 7.4%(42/570) DEGs have been experimentally validated. [score:6]
Fascinating thing is 31.1% DEGs may be directly target by both miRs, and further mechanism study indicated miR-132-3p and miR-212-3p may be participated in brain tumor -induced epilepsy through direct intervention, ceRNA network and indirect adjustment. [score:6]
In addition to Pubmed search, the MalaCards disease database [26] with high credibility and having been used wi dely was also used for further analysis of research potential that miR-132/212 can cause epilepsy, the MalaCards provides 43 affiliated genes found to be associated with the epilepsy, what has specific value in this article is that 32.6% of genes related to epilepsy may be directly targeted by miR-132-3p and miR-212-3p. [score:6]
Experimentally validated target genes of miR-212-3p/miR-132-3p have highly expression in brain. [score:5]
Certainly, two things are worth mentioning when considering further discussion, firstly, miR-132 and miR-212 also presented different expression and miR-132 may be play a major role, each of these miRNAs respectively repress specific targets(diverging nucleotides between miR-132 and miR-212 sequences (see Figure 1A) and have a nonsynchronous status [16, 34]. [score:5]
All the analyze result above, especially the fact that IRAK4 targeted by miR-132/212 can participate in cancer and epilepsy and the survival of brain lower grade glioma (LGG) is significantly affected by both miRs (P=0.002) and its target genes like IRAK4 (p=8.76e-05) (Figure 4B and Figure 4D) remind us whether miR-132-3p and miR-212-3p is the core molecular underlying brain tumor -induced epileptogenesis, To illustrate this hypothesis, GEO (access #: GSE32534), which was the first study of to use formalin-fixed paraffin embedded peritumoral tissues (5-seizure vs. [score:5]
Table 1 and Supplementary Table 1 presented experimentally validated target gene of miR-212-3p/miR-132-3p, there are 951 genes have been validated and all of them have been discussed in various human diseases. [score:5]
So, studying all genes directly target by miR-212/132 is important for us to understand thoroughly how they are involve in pathological mechanism of neurological disorders like epilepsy. [score:4]
MiR-132 and miR-212 were first discovered in mice and display brain and testes tissue-specific patterns of expression [5]. [score:3]
Analysis of biological networks for validated target gene of miR-212-3P/miR-132-3P. [score:3]
So, bioinformatics analyses were used in this study to better understand miR-212/132 gene cluster and its gene regulatory network, and combing the literature review and clinical database to explore the novel and worthwhile studying direction for epilepsy research. [score:3]
miR-212-3p and miR-132-3p work synergistically to control Sox11 expression in the setting of epilepsy [22]. [score:3]
The fact showed in Table 2 and Supplementary Table 2 that most of these genes were highly expressed in brain make the role of miR-212-3p/miR-132-3p as “neurimmiRs” becomes even more prominent. [score:3]
The second one is that miR-132-3p/5p and miR-212-3p/5p, originating from opposite arms of the same pre-miRNA and with different seed sequence, may be involve in another unique role in CNS (figure 1C have showed 5p also have a high concordance of brain tissue-specific expression in human) [35– 37]. [score:3]
Analysis of experimentally validated target gene of miR-212-3P/miR-132-3P. [score:3]
Previous research have found that miR-212/132 have bilateral function depending on cancer types [7], which is in line with the our analytic result, such as high miR-132-3p and low miR-132-3p expression are significantly associated with poor survival in bladder urothelial carcinoma (BLCA) and pancreatic adenocarcinoma (PAAD), respectively. [score:3]
Analysis of all the target gene of miR-212-3P/miR-132-3P. [score:3]
In addition, we found that regulating transcription is the primary biological process of miR-212/132 in enrichment analysis of GO, which is similar to the fact that microRNAs may play important role in transcriptional regulation [43]. [score:3]
Figure 1A/ 1B presented the mature and precursor sequences of miR-132 and miR-212 in human and one example about common target gene of both miRs. [score:3]
The biomolecular information of remaining genes targeted by miR-132-3p and miR-212-3p. [score:3]
In this article, we want to assure whether these genes significantly associated with epilepsy can be directly and indirectly affected by miR-132-3p and miR-212-3p. [score:3]
We would like to acknowledge that the number (3801) of possible target genes occupied a high percentage in genome, by comparison (data no shown), the proportion of genes related to miR-212/132 and have function in epilepsy at the same time is relatively high. [score:3]
Furthermore, miR-132-3p and miR-212-3p share similar mature sequences and common target gene, which is important for further analysis. [score:3]
Computational analysis result of miR-132-3p and miR-212-3p-regulated biomolecular network. [score:2]
Although in the beginning we did not take cancer as the main research object, as data are accumulated and analysis continues, the result demonstrated miR-132-3p and miR-212-3p may participates extensively in human cancer, For experimental validated genes and predicted genes with conservative sites, 34.9 % (15/43) and 38.2% (13/34) pathway are statistically enriched in cancer directly, respectively. [score:2]
Experimental validated Gene-enrichment analysis result of miR-132-3p and miR-212-3p-regulated biomolecular network. [score:2]
Survival analysis reveals that dysregulation of miR-132-3p and miR-212-3p is conspicuously related with poor survival in several human cancer including BLCA, PAAD, KICH and LGG. [score:2]
miR-212/132 gene cluster is one of typical example. [score:1]
miR-132-3p and miR-212-3p may play a critical role in human cancer. [score:1]
Analysis of gene structure and tissue specificity and heterogeneity of miR-212/miR-132. [score:1]
In addition, more evidence derived from GO term and other feature for these DEGs can be found in Supplementary Table 7. (2) Because identical seed sequences, the relative redundancy of miR-132 and miR-212 functions is still an incompletely addressed question. [score:1]
Several Web based tools for “The Cancer Genome Atlas” (TCGA) have been used to visualize, analyze and interpret all the data types whether miR-132-3p and miR-212-3p may be involve in human cancer. [score:1]
The biomolecular information of remaining genes and the role of miR-132, miR-212 and genes participate in epilepsy. [score:1]
“miR-132” and “miR-212” are the most frequently used name in the vast majority of researches, but two mature microRNAs (miR-132-3p/5p and miR-212-3p/5p, respectively) originate from opposite arms of the same pre-miRNA have been found in human genome, so first we need to clarify which one is usually much more abundant in cell and on behalf of the “miR-132/212”, eventually, although there is also a small study miR-132-5p/212-5p oriented, miR-132-3p and miR-212-3p was determined as the predominant by miRbase and sequences alignments in published literature. [score:1]
Besides, oriented to this article focused on epilepsy, literature search (PubMed) was carried out to analyze the exiting role of miR-132 and miR-212 involving in epilepsy. [score:1]
The emerging role of miR-132 and miR-212 participate in epilepsy. [score:1]
Analysis of the emerging role of miR-132-3p and miR-212-3p involved in human cancer. [score:1]
Mature sequence hsa-miR-132-3p and has-miR-212-3p may have a predominant role in nervous tissues. [score:1]
Literature search (pubmed) show that 26.1 % (95/364) (“miR-132”/“miR-132” and“cancer”) and 37.2 %(45/145) (“miR-212”/“miR-212” and“cancer”) studies are related to cancer for miR-132 and miR-212, respectively. [score:1]
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[+] score: 173
To determine the extent to which concomitant down-regulation of miR-212/132 and miR-23a/b and up-regulation of sirt1 observed in aMCI frontal cortex represented a functionally significant relationship, we treated human hNT neuronotypic cells with specific inhibitors of these miRNAs and measured sirt1 protein expression. [score:9]
miR-23a and miR-212 down-regulation protects against Aβ [1−42] induced cell death via sirt1To test whether miR-212 and miR-23a regulation of sirt1 results in neuronal protection, hNT cells were treated with inhibitors of either miRNA independently, or with inhibitors of both miRNAs combined, followed by challenge with Aβ [1−42], which has been shown to induce cell death in these neuronal cells (Counts and Mufson, 2010). [score:9]
Interestingly, inhibition of miR-212, miR-132, miR-23a, or miR-23b individually had no effect on sirt1 expression, but we found that concurrent inhibition of miR-212 and miR-23a resulted in a significant ~100% increase in sirt1 (Figure 4), whereas co -inhibition of miR-132 and miR-23a resulted in a ~40% increase in sirt1 (p < 0.05, data not shown). [score:9]
In particular, Wong and colleagues have previously shown that the miR-212/132 cluster is down-regulated in temporal cortex in AD, and that inhibition of miR-212 and/or miR-132 expression can induce apoptosis in primary neurons after 1 week in culture via activation of a foxo3a -mediated cell death pathway (Wong et al., 2013). [score:8]
Experimental down-regulation of miR-212 and miR-23a in cultured neurons up-regulated sirt1 and provided neuroprotection against Aβ toxicity. [score:7]
hNT cultures were transfected with small miRNA inhibitors (miRCURY LNA inhibitors, Exiqon) specific for miR-212, miR-132, miR-23a, miR-23b, or an inhibitor negative control sequence (Exiqon) (n = 8/treatment group in three independent experiments). [score:7]
Since miRNAs negatively regulate transcript stability, down-regulation of the miR-212/132 and miR-23a/b clusters in frontal cortex would be predicted to promote the stability of their target mRNAs in aMCI. [score:7]
To test whether miR-212 and miR-23a regulation of sirt1 results in neuronal protection, hNT cells were treated with inhibitors of either miRNA independently, or with inhibitors of both miRNAs combined, followed by challenge with Aβ [1−42], which has been shown to induce cell death in these neuronal cells (Counts and Mufson, 2010). [score:6]
miR-212 and miR-23a down-regulation increases sirt1 protein expression in human neuronal cells. [score:6]
Sirt1 mRNA levels were higher in frontal cortex of aMCI subjects but stable in inferior temporal cortex, suggesting a link between miR-212/132 and miR-23a/b down-regulation and reduced transcriptional repression of sirt1 target mRNA. [score:6]
Figure 4 Experimental down-regulation of miR-212 and miR-23a increases sirt1 protein expression. [score:6]
The down-regulation of miR-212/132 in aMCI frontal cortex may initially participate in protective compensatory mechanisms, but with sustained reductions these miRNAs may join a pathological cascade that promotes disease progression through foxo3a. [score:6]
Moreover, the differential roles for this cluster may depend on target binding partners, since miR-212/132 and miR-23a co -inhibition was required for sirt1 activation and neuroprotection. [score:5]
By contrast, miR-23b co -inhibition with miR-212 or miR-132 had no effect on sirt1 expression (data not shown). [score:5]
Scatterplots show that lower miR-212 transcript expression was associated with higher sirt1 transcript expression in (A) frontal cortex (r = −0.81, p < 0.0001), but not in (B) temporal cortex in the subjects examined. [score:5]
Figure 5Experimental down-regulation of miR-212 and miR-23a protects against Aβ [1−42] in a sirt1 -dependent manner. [score:4]
Hence, there are several mechanisms by which miR-212/132 and miR-23a co-regulation of sirt1 expression may promote neuroprotection in the frontal cortex in aMCI. [score:4]
However, two distinct clusters of these miRNAs, miR212/132, and miR 23a/23b, were also significantly down-regulated by ~50% in the frontal cortex of aMCI subjects relative to NCI subjects (Table 3, Figures 1A,B). [score:4]
miR-23a and miR-212 down-regulation protects against Aβ [1−42] induced cell death via sirt1. [score:4]
Box plots show that (A) miR-212 and (B) miR-23a were significantly down-regulated by ~50% in aMCI and by ~60% in AD. [score:4]
In this regard, we replicated the finding that the miR-212/132 cluster is down-regulated in the temporal cortex in AD. [score:4]
Several miRNAs were also significantly down-regulated in AD frontal cortex, including miR-886-3p, miR-132, miR-21, miR-23a, miR-140-3p, miR-212, miR-23b, let-7d, and miR-181a (Table 3). [score:4]
However, we found no reductions in miR-212/132 in this region in aMCI; miR-212/132 was down-regulated in aMCI only in frontal cortex. [score:4]
By contrast, qPCR analysis of temporal cortex revealed that miR-212 and miR-132 expression levels were decreased only in the AD group, whereas miR-23a and miR-23b were unchanged across the clinical diagnostic groups (Table 4). [score:3]
However, co -inhibition of either miR-212 or miR-132 with miR-23a conferred neuroprotection against Aβ [1−42] in a sirt1 -dependent manner. [score:3]
In addition, in our hands experimental inhibition of miR-212 and/or miR-132 had no effect on cell survival of hNT neurons after 48 h in the absence of Aβ [1−42]. [score:3]
Figure 2 Inverse relationship between miR-212 and sirt1 expression in the frontal cortex. [score:3]
Figure 1 Differential expression of miR-212, miR-23a, and sirt1 transcripts in the frontal cortex of aMCI subjects. [score:3]
In summary, our data suggest that the transition from normal cognitive function in aging to a clinical diagnosis of aMCI may involve the suppression of brain microRNA networks such as miR212/132 and miR-23a. [score:3]
Spearman rank correlations were performed to test for relationships between miR-212 and sirt1 expression. [score:3]
By contrast, we found that miR-23a inhibition alone had no effect on Aβ -induced cell death after 48 h, yet was neuroprotective in the presence of miR-212 by activating sirt1. [score:3]
Furthermore, increased sirt1 mRNA expression was significantly associated with decreased miR-212 levels frontal cortex levels, but this association was not found in the temporal cortex (Figure 2). [score:3]
We report that two families of miRNAs, miR-212/132 and miR-23a/b, were down-regulated in frontal cortex in aMCI and AD compared to NCI, yet remained stable in inferior temporal cortex. [score:3]
Hence, we validated these concepts by showing that miR212/132 and miR-23a -mediated neuroprotection against Aβ is prevented by a sirt1-specific inhibitor. [score:3]
Human hNT neuronotypic cells were co -transfected with small inhibitors of miR-212 and 23a or scrambled negative controls (CTL). [score:3]
This rescue effect was reversed by EX527, suggesting that the protective effects of miR-212/23a co-repression was mediated by sirt1. [score:1]
Hence, the activity of the miR-212/132 cluster may be context dependent during the progression of AD. [score:1]
Bar graph shows that Aβ [1−42] treatment resulted in significant cell death that was significantly reduced by miR-212/23a co-repression. [score:1]
However, like miR-212/132, miR-23a levels have been inversely linked to apoptosis. [score:1]
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[+] score: 136
Other miRNAs from this paper: hsa-mir-22, hsa-mir-132
To further understand SIRT1 regulation we tested (in the same LCL RNA preparations) the expression levels of miR-212 [36], miR-132 [35] and miR-22 [37] reported to regulate SIRT1, and observed opposite expression patterns compared with SIRT1 (Fig.   1, Supplementary Fig.   1). [score:6]
Expression levels of miR-132 and miR-212 are downregulated in AD postmortem olfactory bulb and hippocampus. [score:6]
The expression levels of both miR-132 and miR-212 showed a mirror-image of the SIRT1 expression levels in the same LCL cohorts: levels were upregulated in AD LCLs compared with healthy age-matched control LCLs (FD = 1.7; P = 0.014, FD = 2.1; P = 0.036) and, more dramatically, were extremely low in centenarian compared with AD LCLs (FD = 12.9; P = 2.1E-07, FD = 8.6; P = 7.7E-07; Fig.   1b,c). [score:6]
Figure 3Expression levels of miR-132 (a, c) and miR-212 (b, d) in postmortem olfactory bulb (a, b) and hippocampus (c, d) tissues from sporadic Alzheimer’s disease patients and age-matched non-demented controls and their correlations with MMSE scores. [score:5]
The hypothesis that higher miR-212 and miR-132 levels are protective in AD shares common features with our recent suggestion that low peripheral RGS2 expression may serve as an early AD biomarker, while lower RGS2 expression levels were associated with better cognitive scores in AD patients [18]. [score:5]
The expression levels of miR-212 and miR-132 in the hippocampus and olfactory bulb, two brain regions where neurogenesis takes place throughout human life, were downregulated in AD patient postmortem tissues compared with controls (Fig.   3a-d) and were correlated with worse cognitive MMSE scores (Fig.   3e–g). [score:5]
Figure 2Pearson correlation plots for female Alzheimer’s disease MMSE and ADAS cognitive scores and expression levels (2 [−Δct]) of SIRT1, miR-132 and miR-212 in their LCLs. [score:5]
Figure 1Expression levels and correlations of SIRT1, miR-132 and miR-212 in LCLs from female Alzheimer’s disease patients, female healthy controls (in two age groups) and female centenarians. [score:5]
In AD patients, lower SIRT1 expression levels and higher miR-212 and miR-132 LCL expression levels correlated with better cognitive scores (higher MMSE and lower ADAS scores; Fig.   2), suggestive of earlier AD stage. [score:5]
The expression levels of both miR-132 and miR-212 were downregulated in postmortem olfactory bulb (FD = −1.32; P = 0.037 and FD = −1.46; P = 0.025, respectively) and hippocampus tissues (FD = −1.8; P = 0.029 and FD = −2.1; P = 0.004, respectively) from late-onset AD patients (N = 14) compared to non-demented controls (N = 20) (Fig.   3a–d). [score:5]
Note the negative correlation of SIRT1 expression with MMSE but not with ADAS; the negative MMSE correlation agrees with the positive MMSE correlations for miR-132 and miR-212, two miRNAs known to target SIRT1 (see). [score:5]
Patients ADAS score exhibited lack of correlation with SIRT1 expression (Fig.   2d), albeit negative correlations were observed with expression levels of miR-132 (R = −0.67; P = 0.0006) or miR-212 (R = −0.72; P = 0.00014) (Fig.   2e,f). [score:5]
AD LCLs expression levels of SIRT1, miR-132 and miR-212 correlate with patient cognitive scoresThe expression levels of SIRT1, miR-132 and miR-212 in LCLs from female AD patients (N = 22) were examined for correlations with their Mini Mental State Examination (MMSE) scores and AD Assessment Scale (ADAS) scores (Supplementary Table  1). [score:5]
Our results confirm previous findings that miR-212 and miR-132 were downregulated in postmortem hippocampus brain tissues from AD patients [49]. [score:4]
Deletion of miR-132 and miR-212 was shown to induce tau aggregation in mice expressing endogenous or human mutant tau [38], and impair mouse cognitive skills [39]. [score:3]
The expression levels of SIRT1, miR-132 and miR-212 in LCLs from female AD patients (N = 22) were examined for correlations with their Mini Mental State Examination (MMSE) scores and AD Assessment Scale (ADAS) scores (Supplementary Table  1). [score:3]
We observed that miR-212 and miR-132 were upregulated in LCLs from AD patients compared to controls, and were extremely low in centenarian LCLs. [score:3]
Of note, the LCL expression levels of miR-212 and miR-132 exhibited a robust positive Pearson correlation (R = 0.893; P = 6.12E-25; Supplementary Fig.   1c; combined cohorts, N = 69). [score:3]
A negative correlation was observed for the AD postmortem olfactory bulb expression levels of SIRT1 with the patients MMSE cognitive scores (R = −0.54; P = 0.015); while in the hippocampus, both miR-132 and miR-212 showed positive correlations with MMSE scores (R = 0.41; P = 0.037, R = 0.44; P = 0.028; Fig.   3e–g). [score:3]
Corresponding positive correlations were found when comparing MMSE scores and miR-132 (R = 0.47; P = 0.026) and miR-212 LCL expression (R = 0.43; P = 0.046; Fig.   2b,c). [score:3]
Interestingly, AGTR2 activation increases the expression of miR-212 and miR-132 in cardiovascular tissues [58]. [score:3]
SIRT1, miR-132 and miR-212 expression levels in the olfactory bulb and hippocampus are correlated with MMSE scores. [score:3]
SIRT1, miR-132 and miR-212 expression levels in the olfactory bulb and hippocampus are correlated with MMSE scoresThe AD postmortem brain tissue MMSE cognitive scores were explored for detecting correlations with the measured expression levels of the above genes and miRNAs. [score:3]
miR-132, miR-212 and miR-22 were shown to target SIRT1 35– 37. [score:3]
The expression levels of miR-212 and miR-132 exhibited negative Pearson correlations with SIRT1 in the olfactory bulb tissues (Supplementary Fig.   4a,b). [score:3]
In addition, the expression levels of both miR-132 and miR-212 negatively correlated with those of SIRT1 (R = −0.60 P = 4.5E-08; R = −0.49 P = 0.00002; Fig.   1d,e; data were combined for all cohorts, N = 69). [score:3]
Expression levels (2 [−Δct]) are shown for the different LCL groups for: (a) SIRT1 (b) miR-132 (c) miR-212. [score:3]
In the current study, we therefore studied SIRT1, RGS2, miR-132, miR-212 and miR-22 expression levels in LCLs from healthy donors of various age groups, including centenarians, and in LCLs from AD patients. [score:3]
AD LCLs expression levels of SIRT1, miR-132 and miR-212 correlate with patient cognitive scores. [score:3]
In addition, both miR-132 and miR-212 expression levels were negatively correlated with Braak stage scores and BrainNet Europe (BNE) Aβ phase score in AD olfactory bulb tissues (Supplementary Fig.   6). [score:3]
As observed in human LCLs, miR-132 expression levels correlated with those of miR-212 also in the olfactory bulb and hippocampus postmortem tissues (Supplementary Fig.   5a,b). [score:3]
TaqMan® MicroRNA Assay IDs are listed below: MicroRNA Symbol TaqMan™ MicroRNA Assay ID U6 snRNA (Control miRNA Assay) 001973 hsa-miR-22-3p 000398 hsa-miR-132-3p 000457 hsa-miR-212-3p 000515Comparative critical threshold (Ct) values were determined in duplicates for analyzing relative gene and miRNA expression in selected sample groups according to 2 [−ΔCт] (ΔCт = Ct target Gene − Ct reference gene). [score:2]
SIRT1 expression levels were much higher in centenarian compared with AD LCLs, while the opposite was observed for miR-132 and miR-212 in the same cells. [score:2]
TaqMan® MicroRNA Assay IDs are listed below: MicroRNA Symbol TaqMan™ MicroRNA Assay ID U6 snRNA (Control miRNA Assay) 001973 hsa-miR-22-3p 000398 hsa-miR-132-3p 000457 hsa-miR-212-3p 000515 Comparative critical threshold (Ct) values were determined in duplicates for analyzing relative gene and miRNA expression in selected sample groups according to 2 [−ΔCт] (ΔCт = Ct target Gene − Ct reference gene). [score:2]
Our studies of miR-212 and miR-132 expression levels in AD and control LCLs yielded different findings compared with those obtained in postmortem brain tissues; this may reflect cross-talk between the immune system and the brain. [score:2]
This finding is not surprising given the proximal location of miR-212 and miR-132 on human chromosome 17p13.3 (separated by only 263 nucleotides) and was previously reported for chronic lymphocytic leukemia cells [41]. [score:1]
Additionally, miR-132 and miR-212 were reduced in medial frontal gyrus [49], temporal cortex, and gray matter from prefrontal cortex AD postmortem samples [50]. [score:1]
We applied real-time PCR reactions for measuring the expression levels of SIRT1, RGS2, miR-22, miR-132 and miR-212 in postmortem olfactory bulb and hippocampus tissues from AD patients and non-demented age-matched controls. [score:1]
Furthermore, higher miR-132 and miR-212 levels were associated with improved AD patient cognitive scores. [score:1]
Our current observations of higher miR-212 and miR-132 in AD LCLs may thus represent yet another facet of the hypertension/AD link. [score:1]
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[+] score: 87
With respect to the miR-212/132 cluster, inhibition of miR-132 and miR-212 gave rise to the upregulation of PTGS2 and the inhibition of miR-212 resulted in the upregulation of IL15 (Figure  3E). [score:11]
To perform the miRNA inhibitor experiments, we used unlabeled miRCURY LNA™ microRNA Power inhibitors to inhibit miR-99b (reference 4101513), miR-let-7e (reference 4103550), miR-125a (reference 4103094), miR-132 (reference 4103093), miR-212 (reference 4104787) or a control (Negative Control A, reference 199006) Exiqon, Vedbaek, Denmark. [score:7]
Secondly, our results reinforce the key role of the NF-κB transcription factor as a direct regulator of miRNA upregulation, specifically focusing on the miR-99b/let-7e/125a and miR-212/132 clusters. [score:6]
In this study, analysis of miRNA expression changes in osteoclast differentiation from human primary monocytes revealed the rapid upregulation of two miRNA clusters, miR-212/132 and miR-99b/let-7e/125a. [score:6]
The second major conclusion of our study is the role of NF-κB in directly upregulating the miR-212/132 and miR-99b/let-7e/125a clusters, and perhaps other miRNAs. [score:5]
On the other hand, miR-132 targets PTGS2, and miR-212 also targets PTGS2 and IL15 (Figure  3D). [score:5]
In the case of the miRNAs in the miR-212/132 cluster, miR-212 was found to target CX3CR1 and HBEGF, and miR-132 targeted IRF1 and NR4A2. [score:5]
This suggests that the functions of miR-132 and miR-212 are involved in the early events of osteoclastogenesis, since their expression levels are tightly regulated and constrained to the first four days of differentiation. [score:4]
Two miRNA clusters, miR-212/132 and miR- 99b/let-7e/125a, are highly upregulated during the early stages of osteoclastogenesis. [score:4]
Our analysis of the functional effects of the depletion of the miRNAs within the miR-99b/let-7e/125a and miR-212/132 clusters, as well the analysis of their targets, shows that these molecules have a direct role in repressing MO-specific and immunomodulatory genes like TNFAIP3, IGF1R and IL15. [score:4]
In addition, depletion of the miR-212/132 cluster, as well as the analysis of their targets, shows that these elements have a direct role in repressing genes like IRF1 or IL15, which could also shape inflammation. [score:4]
The raw expression data are listed in full in Additional file 1. The array expression data were validated in the samples used (validation set), and in a larger cohort of samples obtained from independent donors (replication set) using Exiqon microRNA LNA™ PCR primer sets (hsa-miR-99b-5p, reference 204367; hsa-miR-125a-5p, reference 204339; hsa-miR-132-3p, reference 204129; hsa-miR-212-3p, reference 204170; hsa-miR-103a-3p, reference 204063). [score:4]
Interestingly, both genes are targeted by the miR-212/132 cluster in our MO -based differentiation mo dels that converge on the set-up of inflammatory or NF-κB programs in different cell types. [score:3]
We transfected primary MOs with specific inhibitors or antagomirs for each of the individual miRNAs contained in the miR-99b/let-7e/125a and miR-212/132 clusters. [score:3]
Analysis of the expression changes of all miRNAs within the miR-99b/let-7e/125a and miR-212/132 clusters showed these are common to all three processes (Figure  4B). [score:3]
miRNAs within two clusters ranked top in terms of the coefficient of change and relative expression levels, specifically miR-99b/let-7e/125a (group I, average fold change = 49.4 between MOs and 48 h post-MCSF/RANKL stimulation) and miR-212/132 (group VI, average fold change = 50.57 between MOs and 48 h post-MCSF/RANKL stimulation) (Figure  1D). [score:3]
We confirmed the overexpression of all the miRNAs within the miR-99b/let-7e/125a and miR-212/132 clusters using quantitative RT-PCR (qRT-PCR) (Figure  1E). [score:3]
Inhibition of miRNAs within the miR-99b/let-7e/125a and miR-212/132 clusters impairs osteoclastogenesis. [score:3]
We carried out these assays in HeLa cells, in which we had previously estimated the expression of high levels of miRNAs of the miR-99b/let-7e/125a and miR-212/132 clusters. [score:2]
This analysis showed that the p65 NF-κB consensus binding site is present in the majority of miRNA TSSs, including the miRNAs within the miR-99b/let-7e/125a and miR-212/132 clusters (Figure  5A). [score:1]
In contrast, miR-212/132 cluster miRNAs peaked at day 3, displaying an increase of around 50-fold (miR132) to 170-fold (miR-212), followed by an approximately 5-fold drop (Figure  1F, bottom). [score:1]
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[+] score: 72
It has been reported that miR-132-3p and miR-212-3p are involved into the neuron morphogenesis, are down-regulated in several brain-related disorders, and also play a role in regulating immune processes (Wanet et al., 2012). [score:5]
6 h miR-132-3p miR-132-5p miR-212-5p SAP30L −0.750 FKBP1B −0.866 KLF4 −0.832 ATP10D −0.881 DHTKD1 −0.801 ABCG1 −0.813 DNPEP −0.790 BARD1 −0.556 TRIM22 −0.531 TTC39C −0.859 Table 3 Correlation coefficients between the expression of fungal DEMs for 12 h and their high-confidence targets. [score:5]
6 h miR-132-3p miR-132-5p miR-212-5p SAP30L −0.750 FKBP1B −0.866 KLF4 −0.832 ATP10D −0.881 DHTKD1 −0.801 ABCG1 −0.813 DNPEP −0.790 BARD1 −0.556 TRIM22 −0.531 TTC39C −0.859 Table 3 Correlation coefficients between the expression of fungal DEMs for 12 h and their high-confidence targets. [score:5]
While expression of miR132-5p did significantly change in NK cells stimulated with A. fumigatus, expression of miR212-5p was significantly increased after 6 h of co-cultivation (p = 0.036). [score:5]
The analysis of differential expression revealed similar regulatory patterns for the 3p and the 5p mature microRNA of both mir-132 and mir-212 after 12 h of stimulation. [score:4]
We performed validation experiments of microRNAs and their predicted target genes revealing fine-tuning regulations by miR-132-5p and miR-212-5p in anti-fungal immune response. [score:4]
12 h miR-132-3p miR-132-5p miR-129-5p miR-212-3p miR-212-5p MTMR1 −0.788 BTN3A2 −0.663 FAM46A −0.545 SP110 −0.778 KLF4 −0.748 SP110 −0.799 FKBP1B −0.934 ADD3 −0.588 MTMR1 −0.863 DHTKD1 −0.865 TTC39C −0.773 CASP6 −0.606 DNPEP −0.828 CCDC170 −0.516 SPN −0.772 TRIM22 −0.690 IFITM2 −0.795 The resulting set of target genes includes genes playing a role in immune response. [score:3]
miR-212/132 expression and functions: within and beyond the neuronal compartment. [score:3]
Furthermore, Wanet et al. (2012) reported that miR-212 and miR-132 are expressed in various immune cells, like macrophages, mast cells and lymphatic endothelial cells. [score:3]
In the presented results, the most immunological relevant target genes were identified for the microRNAs miR-132-5p and miR-212-5p. [score:3]
To demonstrate the relevance of miR132-5p and miR212-5p in additional immune cell populations, experiments stimulating human primary natural killer (NK) cells with A. fumigatus, followed by subsequent microRNA extraction and qPCR -based quantification of miR132-5p and miR212-5p expression were performed. [score:3]
12 h miR-132-3p miR-132-5p miR-129-5p miR-212-3p miR-212-5p MTMR1 −0.788 BTN3A2 −0.663 FAM46A −0.545 SP110 −0.778 KLF4 −0.748 SP110 −0.799 FKBP1B −0.934 ADD3 −0.588 MTMR1 −0.863 DHTKD1 −0.865 TTC39C −0.773 CASP6 −0.606 DNPEP −0.828 CCDC170 −0.516 SPN −0.772 TRIM22 −0.690 IFITM2 −0.795The resulting set of target genes includes genes playing a role in immune response. [score:3]
Figure 4 Further indication for microRNA-target-interactions were collected via western blots and silencing of the microRNAs (A) miR-132-5p and (B–D) miR-212-5p. [score:3]
The immunological relevant targets of miR-212-5p are KLF4, which has been shown to be involved in the response of DCs to fungal infections (Czakai et al., 2016) and to be important for inflammatory immune response (Alder et al., 2008; Rosenzweig et al., 2013), and SPN, a surface molecule of various immune related cells, e. g., T lymphocytes, thymocytes, monocytes, and neutrophiles (Remold-O'Donnell et al., 1987). [score:3]
L. Fischer) with either short interfering single-stranded RNA inhibiting miR-132-5p, miR-212-5p or non-silencing, random RNA (ThermoFisher) at 340 V for 10 ms on day 5 after isolation and then incubated at 37°C and 5% CO [2] for 24 h in culture medium. [score:3]
In addition, miR-132-3p and miR-212-3p share the same seed sequence and thus may have many common target genes. [score:3]
We silenced miR-132-5p and miR-212-5p in separate experiments in DCs generated under identical conditions and in accordance to the co-incubation settings using microRNA inhibitors. [score:3]
Figure 3 Experimental analysis of predicted microRNA-target-interactions by silencing of the microRNAs (A,B) miR-132-5p and (C–F) miR-212-5p using siRNA. [score:3]
In contrast, this is the first study which identified miR-132-5p and miR-212-5p to play major roles in the immune regulation. [score:2]
Although our validation experiments are limited in their extent, we could identify and verify miR-132-5p and miR-212-5p as regulators in DCs during fungal infections. [score:2]
We decided to concentrate on the microRNAs miR-132-5p and miR-212-5p for two reasons: First, only little is known about the roles of these two mircoRNAs in the anti-fungal response. [score:1]
In this way, we found three DEMs (miR-132-3p, miR-132-5p, miR-212-5p) for the 6 h and five DEMs (miR-129-5p, miR-132-3p, miR-132-5p, miR-212-3p, miR-212-5p) for the 12 h samples (Figure 1). [score:1]
This observation indicates the general relevance of miR212-5p in various cell populations of the innate immunity. [score:1]
While miR-132-3p has been linked to A. fumigatus infections before (Das Gupta et al., 2014), it is also involved in different immune processes together with miR-212-3p (Wanet et al., 2012). [score:1]
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[+] score: 70
Panel D shows the effect of miR-212 mimic and inhibitor on cell number and panel E shows phase contrast light microscopic images of cells transfected with negative control (NC), miR-212 mimic and miR-212 inhibitor. [score:5]
Prior work has shown that miR-132 and miR-212 regulate cardiomyocyte hypertrophy by targeting FoxO3 and calcineurin-A/NFAT signaling [14]. [score:4]
MiR-132 and miR-212 are expressed in neurons where they regulate excitability [6], and a body of literature has demonstrated roles of these miRNAs in synaptic plasticity [7], [8], [9]. [score:4]
In order to examine in which tissue compartment miR-132 and miR-212 are expressed, we used control and smooth muscle-specific Dicer knockout (KO) mice. [score:4]
MiR-132 and miR-212 have identical seed sequences and are therefore predicted to target an overlapping set of mRNAs. [score:3]
0116784.g002 Figure 2Control mice and mice with smooth muscle-specific deletion of Dicer (KO) were used to examine the contribution of smooth muscle cells to miR-132 and miR-212 expression in the bladder (panels A through C). [score:3]
We next searched the literature for validated miR-132/212 targets and selected nine for which correlations with miR-132 and miR-212 were examined. [score:3]
MiR-132 and miR-212 inhibitors (AM10166, AM10340, Ambion, Thermo Scientific, Pittsburgh, PA, USA; 10 nM and 100 nM), mimics (Mission miRNA: Sigma-Aldrich, St. [score:3]
Largely similar results for all drugs used in Fig. 3E through G were obtained for miR-212 with one exception; brefeldin A significantly suppressed miR-212 (p = 0.045, not shown). [score:3]
Panel C shows the detrusor to mucosa expression ratio of miR-132 and miR-212 in control and KO bladders. [score:3]
The expression of miR-132 in the bladder is higher than that of miR-212, making the contribution of miR-212 to the observed correlations modest. [score:3]
Here we demonstrate that transfection of miR-212 mimic and inhibitor has opposing effects on detrusor cell number in vitro. [score:3]
Panel A shows miR-212 expression in control and KO mice following separation of the detrusor and mucosa using micro-dissection. [score:3]
Control mice and mice with smooth muscle-specific deletion of Dicer (KO) were used to examine the contribution of smooth muscle cells to miR-132 and miR-212 expression in the bladder (panels A through C). [score:3]
These effects were apparent in bright field images of cells after transfection of miR-212 mimic and inhibitor compared to negative control (NC, Fig. 7E). [score:2]
Panel C shows effect of miR-212 mimic and inhibitor (100 nM of each) on cell viability using the MTT assay. [score:2]
MiR-212 mimic was found to reduce both viability and cell number (Fig. 7C and D), whereas the inhibitor increased cell number (Fig. 7D). [score:2]
The normalized sum of miR-132 and miR-212 in bladders from sham-operated, obstructed (10 days and 6 weeks) and de-obstructed rats was correlated with the mRNA levels for Mecp2 (A), Ep300 (B), Pnkd (C), Jarid1a (D), Sh3bp5 (E), Ripk2 (F), Foxo3 (G), Pten (H) and Rasa1 (I). [score:1]
In humans, miR-132 and miR-212 are derived from a bicistronic precursor transcribed from chromosome 17 [5]. [score:1]
The corresponding star sequences (5p) were similarly induced (rno-miR-132-5p: 3.2-fold, p = 0.0005; rno-miR-212-5p: 4.0-fold, p = 0.0001). [score:1]
We found that the detrusor:mucosa ratios of both miR-132 and miR-212 were reduced in Dicer KO bladders (Fig. 2C). [score:1]
A similar trend was seen for miR-212 (not shown). [score:1]
Work in the heart, finally, has shown that miR-132 and miR-212 are involved in hypertrophy [14]. [score:1]
Recent work has highlighted roles of miR-132 and miR-212 in non-neural tissues. [score:1]
Creb binding to two CRE motifs upstream of miR-212 and one CRE motif upstream of miR-132 has been demonstrated by chromatin immunoprecipitation in rat neurons [6]. [score:1]
Dicer KO affects many miRNAs and the reductions of miR-132 and miR-212 were small, so we cannot rule out a modulating influence of miR-132/212 on Ache in the bladder. [score:1]
Microarrays using bladders obstructed for 10 days and at 6 weeks as well as de-obstructed and sham-operated bladders (GEO: GSE47080) demonstrated induction of miR-132 (rno-miR-132-3p) and of miR-212 (rno-miR-212-3p) in bladder outlet obstruction and a return towards control level on de-obstruction (Fig. 1A, B). [score:1]
0116784.g004 Figure 4The normalized sum of miR-132 and miR-212 in bladders from sham-operated, obstructed (10 days and 6 weeks) and de-obstructed rats was correlated with the mRNA levels for Mecp2 (A), Ep300 (B), Pnkd (C), Jarid1a (D), Sh3bp5 (E), Ripk2 (F), Foxo3 (G), Pten (H) and Rasa1 (I). [score:1]
It is however unlikely that that miR-132 and miR-212 are responsible for the neuro-effector transmission defect that we have previously reported in Dicer KO bladders [3]. [score:1]
Despite the fact that miR-132 and miR-212 are Dicer -dependent miRNAs, only small (≈24%) reductions in miR-212 (p = 0.03, Fig. 2A) and miR-132 (p = 0.08, not shown) were observed in Dicer KO detrusor. [score:1]
MiR-132 and miR-212 are increased in the detrusor and not in the mucosa following outlet obstruction. [score:1]
These latter studies showed that transfection of miR-132 mimic led to reduced smooth muscle cell viability, proliferation and migration [21], suggesting the existence of a negative feedback loop in which growth-promoting stimuli increase miR-132 and miR-212 which in turn limit cell proliferation. [score:1]
We used the normalized sum of miR-132 and miR-212 because these miRNAs have the same seed sequences, but one may raise arguments against this approach. [score:1]
Induction of miR-132 and miR-212 following bladder outlet obstruction. [score:1]
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[+] score: 36
For the latent stage, 18 consistently differentially expressed mature miRNA sequences were identified: 8 were up-regulated (miR-212-3p, miR-21-5p, miR-132-3p, miR-20a-5p, miR-17-5p, miR-27a-3p, miR-23a-3p, miR-146a-5p) and 10 were down-regulated (miR-139-5p, miR-551b-3p, miR-33-5p, miR-708-5p, miR-7a-5p, miR-935, miR-138-5p, miR-187-3p, miR-30e-3p, miR-222-3p) (Table  2). [score:9]
For the acute stage, 9 mature miRNA sequences were identified as consistently differentially expressed: 8 were up-regulated (miR-132-3p, miR-21-5p, miR-21-3p, miR-212-3p, 2137, miR-711, miR-882 and miR-142-5p) and one was down-regulated (miR-302b-5p) (Table  2). [score:9]
For the chronic stage, 9 mature miRNA sequences were identified: 8 were up-regulated (miR-146a-5p, miR-23a-3p, miR-135b-5p, miR-21-5p, miR-132-5p, miR-132-3p, miR-210-3p, and miR-212-5p) and one was down-regulated (miR-551b-3p) (Table  2). [score:7]
The most common up-regulated miRNAs across the analyzed set of expression profiles were miR-21-5p (15 profiles), followed by miR-132-3p, miR-23a-3p, miR-212-3p, miR-146a-5p, miR-27a-3p, miR-129-5p, miR-203a-3p, miR-17-5p, miR-19a-3p (Supplementary Table  S4). [score:6]
Deregulation of these miRs may represent the interplay between neuronal cell death and neuroprotection, as both miR-21 and miR-212/132 have been previously implicated in these processes in the brain 31, 55. [score:2]
Both miR-21 and the cluster of miR-212/132 have been implicated in epilepsy and various neurologic disorders 53, 54. [score:1]
Noteworthy, miR-21 appeared in all 3 stages, as well as miRNAs from miR-212/132 cluster. [score:1]
The only 3 common miRNAs that were found between all 3 stages of epileptogenesis were miR-21–5p, miR-132–3p and miR-212–3p. [score:1]
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[+] score: 35
ARB treated patients (n = 16) revealed a significant attenuation of miR-132 expression (0.55-fold), as well as a tendency for miR-212 downregulation (0.64-fold), as compared to non-ARB -treated patients (miR-132; 0.93 and miR-212; 1.01) (n = 16) (Figure 5B). [score:5]
Despite these limitations, we observed a significant downregulation of miR-132, as well as a robust attenuation of miR-212 in the ARB -treated patients. [score:4]
Interestingly, even though the ET-1 -induced hypertension had a much shorter duration than the sustained hypertension induced by AngII, both miR-132 and miR-212 were upregulated at a point in time when blood pressure was not (Figure 4). [score:4]
Furthermore, miR-132 was found to be significantly upregulated in the plasma of AngII -induced hypertensive animals, whereas no regulation was observed for plasma miR-212 levels compared to the control rats (Figure 2B). [score:4]
Even though miR-132 and miR-212 are expressed from the same precursor, we observed independent regulation in the different tissues in response to the same AngII infusion. [score:4]
For example, miR-132 and miR-212 are clustered closely in the genome and are transcribed together under the regulation of cAMP response element binding protein [8], which is a known AngII regulated gene [9, 10]. [score:3]
Lack of miR-212 upregulation in the plasma of AngII -induced hypertensive rats compared to control rats might be caused by the low concentration and high variability of the miR-212 levels found in the plasma. [score:3]
Since the miR-132 gene is clustered with the miR-212 gene and they are likely expressed together [21], we included miR-212 in further analyses. [score:3]
Since no anti-miR experiments have been conducted, it has not been possible to deduce the specific cause and effect relationship; however, the regulation of miR-132 and miR-212 is likely biological important, because although rats and humans share biological features in blood pressure control, they have multiple differences in the molecular subtypes of ion channels, receptors and signaling pathways in blood vessel cells. [score:2]
Further studies are necessary to assess the relative biological and pharmacological impact of individual miR-132 and miR-212 levels on systemic blood pressure, in the heart, arterial wall and kidney. [score:1]
Thus, AT [1]R activation in rats increases miR-132 and miR-212, while blocking the AT [1]R decreases miRNA levels in humans. [score:1]
Our results suggest that miR-132 and miR-212 are involved in AngII -induced Gαq-signaling pathway leading to hypertension. [score:1]
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[+] score: 31
In 2015, Kottawwata et al.  published a study in Biology of Reproduction journal, where the authors hypothesized that fetal hCG could increase the expression of mir-212 and downregulate the expression of OLFM1 and CTBP in favor of the embryo attachment to genital tract. [score:8]
The hCG suppressed proteins OLFM1 and CTBP1 in both human endometrial and fallopian epithelial cell lines used, however, hCG stimulated the expression of mir-212 and downregulated OLFM1 in both cell lines, but not CTBP1. [score:8]
Thus, hCG leads to downregulation of OLFM1 and CTBP1 expression in the fallopian and endometrium epithelial cell by stimulation of mir-212[42]. [score:6]
It is interesting that hCG induces the expression of mir-212 which in turn regulates the expression of OLFM1 and CTB1in mouse granulosa cells. [score:6]
From the aspect of implantation, a great role seems to be played by mir-212 and the regulation on the Olfactomedin 1 (OLFM1) and C-terminal -binding protein (CTBP); all of them are under the regulatory control of Luteinizing hormone (LH) / Follicle stimulation hormone (FSH) [39]. [score:3]
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[+] score: 31
When stimulated with LPS, human macrophages have been shown to up-regulate miR-132 [46] and both miR-132 and miR-212 can regulate the expression of proteins involved in the inflammatory response [47]. [score:7]
We chose miR-132* and miR-212 among the seven miRNAs up-regulated in exudated neutrophils for validation of the expression pattern between PMNs isolated from blood and the PMNs from skin window (Fig. 5B). [score:6]
3′ UTR analysis of the mRNAs encoding the pro-apoptotic proteins APAF1, CASP8 and FADD reveals possible targets for miR-212, miR-132, and miR-760, which are all up-regulated in exudated neutrophils compared to peripheral blood PMNs (table 4). [score:5]
When comparing the array data from PMNs and skin window PMNs, we found seven differentially regulated miRNAs (miR-297, miR-212, miR-132, miR-132*, miR-1915*, miR-760, and miR-27a*) that were all up-regulated in the extravasated neutrophils. [score:5]
Interestingly, all seven miRNAs (miR-297, miR-212, miR-1915*, miR-132, miR-27a*, miR-760 and miR-132*) were up-regulated in the skin window neutrophils (Fig. 4 and Table S2). [score:4]
Although best described in neuronal development, miR-212/132 has also been associated with immune regulation. [score:3]
Interestingly, miR-212 and miR-132 are part of the same primary transcript and have the same seed region. [score:1]
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[+] score: 28
MeCP2 acts to repress expression of miR-212 in the dorsal striatum in an activity dependent manner, and also controls the expression of brain-derived neurotrophic factor (BDNF), a protein with an established role in modulating cocaine-related behaviors (Horger et al., 1999; Graham et al., 2007). [score:5]
In rats with a history of extended access to cocaine, the microRNA miR-212 was up-regulated in the dorsal striatum (Hollander et al., 2010), a brain region that becomes progressively engaged with prolonged drug experience (Letchworth et al., 2001; Porrino et al., 2004). [score:4]
miR-212 can also feedback to repress expression of MeCP2, and these two transcriptional regulators are involved in a negative homeostatic balancing act (Im et al., 2010). [score:4]
Virally -mediated over -expression of miR-212 in the dorsal striatum decreased the motivation to consume cocaine, but only under extended access conditions (Hollander et al., 2010). [score:3]
MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212. [score:3]
Inhibition of miR-212 signaling in this region produced the opposite effect, and facilitated compulsive cocaine self-administration. [score:3]
miR-212 is induced in response to CREB signaling (Vo et al., 2005), and exerts its effects by potentiating the activity of CREB (Hollander et al., 2010), revealing a novel feedforward mechanism whereby miR-212 is seemingly able to protect against the development of compulsive cocaine intake. [score:2]
Finally, the identification of factors that regulate escalating drug use both on a synaptic level (e. g., persistent impairments in NMDAR -dependent LTD in the NAc) and on a molecular level (e. g., striatal signaling pathways involving miR-212 and MeCP2) are bringing us closer to understanding the mechanisms that underpin the transition to addiction (Hollander et al., 2010; Im et al., 2010; Kasanetz et al., 2010). [score:2]
It would be of great interest to ascertain whether transcriptional regulation by miR-212/MeCP2 is involved in the mechanism of “recovery” observed in non-addict rats (Kasanetz et al., 2010), and this may bring us closer to understanding factors that underlie both vulnerability and resilience to addiction (Ahmed, 2012). [score:2]
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[+] score: 25
Specifically, five miRNAs (miR-26b, miR-26a, miR-212, miR-107, and miR-103) were upregulated and twelve miRNAs (miR-125b, miR-141, miR-144, miR-164, miR-145, miR-143, miR-15b, miR-16, miR-186, let-7b, let-7a3, and miR-128) were downregulated. [score:7]
The most representative ones were miR-212, miR-026a, miR-150, miR-152, miR-191, and miR-192, which were upregulated in pituitary adenomas, while miR-024-1 and miR-098 were downregulated in tumor samples. [score:7]
GnRH induces expressions of miR-132 and miR-212 in L βT2 pituitary gonadotrope cells to regulate cellular morphology and migration. [score:4]
miR-212 is strongly upregulated in pituitary adenomas [41]. [score:4]
Putative targets of miR-212 include death effector domain-containing protein (DEDD), a protein involved in apoptotic signaling [82], as well as other proteins participating in apoptosis. [score:3]
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[+] score: 25
Overexpression of miR-212 inhibits CRC cell migration and invasion in vitro and pulmonary metastasis in vivo by targeting expression of MnSOD, which is required for downregulation of epithelial markers and upregulation of mesenchymal markers in CRC cells. [score:15]
Therefore, miR-212 could be a prognostic marker for CRC patients to predict their survival, and both miR-212 and MnSOD might also be therapeutic targets for cancer. [score:3]
107, 108 MiR-212 is significantly downregulated in human CRC tissues due to both promoter hypermethylation and loss of heterozygosity. [score:3]
105, 106 Other important miRNAs involved in regulating metastasis include miR-9 and miR-212. [score:2]
105, 106 Other important miRNAs involved in regulating metastasis include miR-9 and miR-212. [score:2]
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[+] score: 24
Other miRNAs from this paper: hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-27a, hsa-mir-30a, hsa-mir-32, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-107, hsa-mir-129-1, hsa-mir-30c-2, hsa-mir-139, hsa-mir-181c, hsa-mir-204, hsa-mir-181a-1, hsa-mir-222, hsa-mir-15b, hsa-mir-23b, hsa-mir-132, hsa-mir-138-2, hsa-mir-140, hsa-mir-142, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-154, hsa-mir-186, rno-mir-324, rno-mir-140, rno-mir-129-2, rno-mir-20a, rno-mir-7a-1, rno-mir-101b, hsa-mir-29c, hsa-mir-296, hsa-mir-30e, hsa-mir-374a, hsa-mir-380, hsa-mir-381, hsa-mir-324, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-15b, rno-mir-17-1, rno-mir-18a, rno-mir-19b-1, rno-mir-19b-2, rno-mir-19a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-27a, rno-mir-29c-1, rno-mir-30e, rno-mir-30a, rno-mir-30c-2, rno-mir-32, rno-mir-92a-1, rno-mir-92a-2, rno-mir-93, rno-mir-107, rno-mir-129-1, rno-mir-132, rno-mir-138-2, rno-mir-138-1, rno-mir-139, rno-mir-142, rno-mir-146a, rno-mir-154, rno-mir-181c, rno-mir-186, rno-mir-204, rno-mir-212, rno-mir-181a-1, rno-mir-222, rno-mir-296, rno-mir-300, hsa-mir-20b, hsa-mir-431, rno-mir-431, hsa-mir-433, rno-mir-433, hsa-mir-410, hsa-mir-494, hsa-mir-181d, hsa-mir-500a, hsa-mir-505, rno-mir-494, rno-mir-381, rno-mir-409a, rno-mir-374, rno-mir-20b, hsa-mir-551b, hsa-mir-598, hsa-mir-652, hsa-mir-655, rno-mir-505, hsa-mir-300, hsa-mir-874, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, rno-mir-466c, rno-mir-874, rno-mir-17-2, rno-mir-181d, rno-mir-380, rno-mir-410, rno-mir-500, rno-mir-598-1, rno-mir-674, rno-mir-652, rno-mir-551b, hsa-mir-3065, rno-mir-344b-2, rno-mir-3564, rno-mir-3065, rno-mir-1188, rno-mir-3584-1, rno-mir-344b-1, hsa-mir-500b, hsa-mir-374c, rno-mir-29c-2, rno-mir-3584-2, rno-mir-598-2, rno-mir-344b-3, rno-mir-466b-3, rno-mir-466b-4
Finally, other subsets of miRNAs were either up-regulated (miR-23a-3p, miR132-3p, miR-146a-5p, miR-154-3p, miR-181d-5p, miR-212-3p, miR-212-5p, miR-344b-5p, miR-380-3p, miR-410-3p, miR-433-3p and miR-3584; Fig. 2, Supplementary Fig. S4), or down-regulated (miR-29c-5p, miR-30a-5p, miR-30c-2-3p, miR-30e-3p, miR-138-5p, miR-140-3p, miR-551b-3p and miR-652-3p; Fig. 2, Supplementary Fig. S5) during all phases of the disease. [score:9]
Moreover, we and Gorter et al. 24 observed the up-regulation of miR-212-5p, whereas we and Bot et al. 23 observed the up-regulation of miR-433-3p. [score:7]
Cluster 1, composed by miR-674-3p, miR-505-3p and miR-212-5p, was up-regulated during epileptogenesis (4 and 8 days after SE). [score:4]
In fact, the expression patterns of miR-20b-5p, miR-142-3p, miR-181d-5p, miR-212-5p, miR-344b-5p and miR-674-3p were identical to those observed using the microarray, and those of miR-21-5p and miR-146a-5p were very similar, although not identical (Fig. 4). [score:3]
Cluster 4, together with cluster 1 (that includes miR-674-3p, miR-505-3p and miR-212-5p) and cluster 5 (including miR-144b-5p and miR-20b-5p), may also strongly influence neuronal activity. [score:1]
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[+] score: 23
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26b, hsa-mir-27a, hsa-mir-31, hsa-mir-33a, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-147a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-221, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-132, hsa-mir-142, hsa-mir-145, hsa-mir-152, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-127, hsa-mir-134, hsa-mir-200c, hsa-mir-106b, hsa-mir-361, hsa-mir-148b, hsa-mir-20b, hsa-mir-410, hsa-mir-202, hsa-mir-503, hsa-mir-33b, hsa-mir-643, hsa-mir-659, bta-let-7f-2, bta-mir-103-1, bta-mir-148a, bta-mir-21, bta-mir-221, bta-mir-26b, bta-mir-27a, bta-mir-99a, bta-mir-125a, bta-mir-125b-1, bta-mir-145, bta-mir-199a-1, bta-mir-27b, bta-mir-30b, bta-mir-31, bta-mir-127, bta-mir-142, bta-mir-20b, bta-let-7d, bta-mir-132, bta-mir-148b, bta-mir-200c, bta-mir-22, bta-mir-23a, bta-mir-29b-2, bta-mir-361, bta-let-7g, bta-mir-24-2, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-25, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-125b-2, bta-mir-34a, hsa-mir-708, hsa-mir-147b, hsa-mir-877, hsa-mir-940, hsa-mir-548j, hsa-mir-302e, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-100, bta-mir-106b, bta-mir-130a, bta-mir-134, bta-mir-147, bta-mir-152, bta-mir-153-1, bta-mir-153-2, bta-mir-182, bta-mir-24-1, bta-mir-199a-2, bta-mir-202, bta-mir-212, bta-mir-224, bta-mir-33a, bta-mir-33b, bta-mir-410, bta-mir-708, bta-mir-877, bta-mir-940, bta-mir-29b-1, bta-mir-148c, bta-mir-503, bta-mir-148d
For this a total of six miRNAs representing those whose expression was induced (miR-212, miR-182 & let-7 g) or suppressed (miR-100, miR-877 and miR-200c) due to hyperstimulation were selected for detecting their expression in exosome and Ago2 fractions. [score:7]
Among the up-regulated miRNAs, miR-212 and miR-148b-5p showed the highest fold change regulation. [score:5]
Moreover, these two miRNAs (miR-212, −132) were found to be significantly up-regulated in preovulatory mouse mural granulosa cells following LH/hCG induction [41] indicating their potential involvement in follicular development in those species. [score:5]
For instance, miR-212 & miR-132 were reported to be involved in regulating follicular development [39, 40]. [score:3]
unst) TGF-beta signaling pathway miR-106b, −132, −148b-5p, −182, −212, −374a, −548j 1.75E-07 TGFBR2, TGFB2, SMAD2, SMAD3, SMAD4, BMPR2 Axon guidance miR-22-5p, −30b, −31, −33a-3p, −182, −132, −550a 2.85E-06 EFNB1, DCC, EPHB4, EPHA3, PLXNA1, PAK4 MAPK signaling pathway miR-30b, −106b, −132, −182, −212, −548j, −202-5p 6.43E-05 MAP3K1, MAP3K5, KRAS, MRAS, GRB2, FGF7 Endocytosis miR-33a-3p, −106b, −182, −374a, −374b, −202-5p 3.83E-04 RAB11FIP4, RAB11FIP2, EEA1, IGF1R, EPS15, EPN Colorectal cancer miR-30b, −33a-3p, −106b, −132, −212, −384, −494 5.94E-04 SOS1, FZD3, SMAD2, DCC, MAPK1, BAX Pathways in cancer miR-33a-3p, −107, −132, −212, −494, −495, −548j 5.95E-04 E2F1, FGF18, WNT16, FGF7, PTEN, MITF Wnt signaling pathway miR-132, −212, −33a-3p, −494, −940, −495, −548j, −107 6.73E-04 LRP5, LRP6, TCF7, PLCB4, DVL3, WNT1, WNT5A Neurotrophin signaling pathway miR-106b, −30b, −940, −182, −212, −107, 0.001267 PIK3R2, NTRK2, NTRK3, RPS6KA6, IRS1, RAC1 Oocyte meiosis miR-212, −132, −940, 495, −595, −107 0.003369 CDC27, CPEB1, PRKACB, FBXW11, MAPK1, RPS6KA3 GnRH signaling pathway miR-940, −495 0.007085 PRKCA, SRC, MAP3K2, MAPK14, GRB2, MAP3K3 Underexpressed miRNAs (Hyp vs. [score:3]
[1 to 20 of 5 sentences]
20
[+] score: 23
Other miRNAs from this paper: hsa-mir-132, hsa-mir-146a, hsa-mir-155, hsa-mir-330, hsa-mir-505
These target sequences are localized in the IL-1 coding sequences and are also present in the plasmid used in the overexpression experiments in Figure 5. miR-132 and miR-212 have similar mature sequences, share the same seed region, apparently target the same mRNAs, and are involved in the development and function of neurons and immune cells [53]. [score:8]
We tested the effects of miR-132 and miR-212 inhibitors to determine whether the IL-1 translational block in astrocytes can be released by them. [score:5]
miR-132, miR-212 or the proteasome inhibitor lactacystin do not affect the expression of IL-1 in human astrocytes. [score:5]
Anti-miR-132, anti-miR-212 and control miR inhibitor (Negative Control #1) were purchased from Applied Biosystems. [score:3]
Table S2 Alignment of sequences (miR-212, miR-132, IL-1α and IL-1β). [score:1]
Alignment of miR-212, miR-132 and IL-1α, IL-1β sequences is provided in Table S2. [score:1]
[1 to 20 of 6 sentences]
21
[+] score: 21
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-96, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-192, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-211, hsa-mir-181a-1, hsa-mir-214, hsa-mir-217, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-145, hsa-mir-152, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-136, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-34c, hsa-mir-26a-2, hsa-mir-302b, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-328, hsa-mir-335, hsa-mir-133b, hsa-mir-409, hsa-mir-484, hsa-mir-485, hsa-mir-486-1, hsa-mir-490, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-512-1, hsa-mir-512-2, hsa-mir-506, hsa-mir-509-1, hsa-mir-532, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-33b, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-1224, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-802, hsa-mir-509-2, hsa-mir-509-3, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-320e, hsa-mir-548x, hsa-mir-378c, hsa-mir-4262, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-203b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-486-2, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Tang Y. Banan A. Forsyth C. B. Fields J. Z. Lau C. K. Zhang L. J. Keshavarzian A. Effect of alcohol on miR-212 expression in intestinal epithelial cells and its potential role in alcoholic liver disease Alcohol. [score:5]
Further studies are needed to clarify the mechanism of miR-212 upregulation in the intestine and colon of ALD. [score:4]
Colonic tissues from patients with ALD showed enhanced expression of miR-212 and also showed a concomitant decreased ZO-1 protein level. [score:3]
This study suggests that increased miR-212 in the small intestine and colon targets tight junction protein and negatively affects intestinal barrier function in ALD [104]. [score:3]
Increased levels of miR-212 in the intestine were reported with alcohol feeding and this increased miR-212 targets tight junction proteins like Zona Occludens-1 (ZO-1). [score:3]
Expression of miR-212 was found to be highly abundant in intestine and colon compared to other organ like heart, liver, and kidney [104]. [score:2]
MiR-132 and miR-212 are encoded by a single gene [103] and the role of miR-212 in the intestine barrier dysfunction is discussed in “microRNAs and intestinal tight junctions in ALD” section. [score:1]
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[+] score: 20
We validated the expression of these five selected miRNAs by qRT-PCR in the 10 cell lines and found that miR-146a was higher expressed in 3 triple -negative breast cancer cell lines: MDA-MB-231, MDA-MB-436 and SUM1315-BRCA1 (Fig. 1c), that miR-153 was higher expressed in 4 triple -negative breast cancer cell lines: MDA-MB-436, SUM1315MO2, SUM149PT and HCC1937 (Fig. 1d), and that miR-146b-5p, miR-132 and miR-212 were expressed in all 10 cell lines at different levels (Fig. S1) without a significant difference between the triple -negative, luminal or benign cell lines. [score:9]
From the selected miRNAs (listed in Table S4), we chose five miRNAs, i. e., two miRNAs (miR-146a and miR-146b-5p) that were previously found to be over-expressed in breast tumors and to down-regulate BRCA1 expression [18] and three miRNAs (miR-132, miR-212, miR-153) that were most frequently predicted to interact with the 3′-UTR of BRCA1. [score:8]
Expression level of miR-146b-5p, miR-132 and miR-212 in mammary cell lines. [score:3]
[1 to 20 of 3 sentences]
23
[+] score: 20
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-23a, hsa-mir-25, hsa-mir-26a-1, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, hsa-mir-198, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-27b, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-142, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-186, hsa-mir-188, hsa-mir-193a, hsa-mir-194-1, hsa-mir-320a, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-194-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-362, hsa-mir-369, hsa-mir-375, hsa-mir-378a, hsa-mir-382, hsa-mir-340, hsa-mir-328, hsa-mir-342, hsa-mir-151a, hsa-mir-148b, hsa-mir-331, hsa-mir-339, hsa-mir-335, hsa-mir-345, hsa-mir-196b, hsa-mir-424, hsa-mir-425, hsa-mir-20b, hsa-mir-451a, hsa-mir-409, hsa-mir-484, hsa-mir-486-1, hsa-mir-487a, hsa-mir-511, hsa-mir-146b, hsa-mir-496, hsa-mir-181d, hsa-mir-523, hsa-mir-518d, hsa-mir-499a, hsa-mir-501, hsa-mir-532, hsa-mir-487b, hsa-mir-551a, hsa-mir-92b, hsa-mir-572, hsa-mir-580, hsa-mir-550a-1, hsa-mir-550a-2, hsa-mir-590, hsa-mir-599, hsa-mir-612, hsa-mir-624, hsa-mir-625, hsa-mir-627, hsa-mir-629, hsa-mir-33b, hsa-mir-633, hsa-mir-638, hsa-mir-644a, hsa-mir-650, hsa-mir-548d-1, hsa-mir-449b, hsa-mir-550a-3, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-454, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-708, hsa-mir-216b, hsa-mir-1290, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-3151, hsa-mir-320e, hsa-mir-378c, hsa-mir-550b-1, hsa-mir-550b-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j, hsa-mir-486-2
Consistently, CCL3 and CCL4 were found up-regulated in high miR-212 expression cases and, as genes that belong to the CCL2-4/CXCL1/8 class of chemokines, they are involved in T- and NK-cell chemotaxis. [score:6]
In addition, increased expression of miR-212, miR-25 and/or miR-203 has been associated with a favorable overall survival, event-free and relapse-free survival in AML patients independent of cytogenetic subtypes [65, 116– 118]. [score:3]
An enhanced chemotaxis of immune cells might contribute to their anti-leukemic effects and result in a better response to chemotherapy treatment in patients with high miR-212 expression [65, 116– 118]. [score:3]
Interestingly, AML patients with high expression levels of miR-212 displayed a significant enrichment of genes involved in the immune response. [score:3]
Gene expression profiling showed that the miRNAs miR-132 and miR-212 affected the Rb or TP53 signaling pathway, which may explain the clinical observation [29]. [score:3]
Moreover, miR-132 and miR-212 expression was lower in progressive CLL patients compared with stable CLL patients [29]. [score:2]
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24
[+] score: 20
Functional gene ontology (GO) annotation study for biological process conducted on the list of putative targets obtained for miRNAs de-regulated in DC after Mtb infection, namely miR-155-5p, miR-155-3p, miR-29b-1-5p, miR-150-5p, miR-146a-5p, miR-212-5p and miR483-5p. [score:4]
S1 Table Functional gene ontology (GO) annotation study for biological process conducted on the list of putative targets obtained for miRNAs de-regulated in DC after Mtb infection, namely miR-155-5p, miR-155-3p, miR-29b-1-5p, miR-150-5p, miR-146a-5p, miR-212-5p and miR483-5p. [score:4]
In addition to miR-155, we identified several others miRNAs induced in Mtb infected DC, as miR-155*, miR-29b-1*, miR-150, miR-146a, miR-212 and miR-483-5p, whose expression was also found altered in patients affected by pulmonary TB [14– 28]. [score:3]
Gene Ontology annotation for the list of putative targets of miR-155, miR-155*, miR-29b-1*, miR-150, miR-146a, miR-212 and miR-483-5p was obtained from miRWalk (http://www. [score:3]
Interestingly, among miRNAs de-regulated in TB patients and validated by real time PCR or similar techniques [14– 28], seven miRNAs—namely miR-155, miR-155*, miR-29b-1*, miR-150, miR-146a, miR-212 and miR-483-5p –were found altered in Mtb-infected DC (Figs 1 and 2A). [score:2]
MiR-150 and miR-212 induction was maintained over time, while 24 hour post-infection, miR-29b-1* decreased and miR-483-5p peaked (Fig 2A). [score:1]
On the contrary, although miR-29b-1*, miR-150, miR-212 and miR-483-5p induction was confirmed by q-PCR experiments, their kinetic of induction does not perfectly mirror that showed by microarray analysis (Figs 1 and 2). [score:1]
In particular, by taking advantage of the performed GO analysis, we noticed that, while miR-29b-1*, miR-150, miR-212 and miR-483-5p showed an enrichment in GO terms important for host-response to Mtb infection such as ubiquitin, proteasome degradation and endocytosis, only miR-155, miR-155* and miR-146a displayed a significant enrichment in biological processes linked to autophagy, a process deeply implicated in Mtb infection control [29, 30] (S2 Table). [score:1]
Furthermore, microarray data indicated that Mtb induced miR-29b-1*, miR-150, miR-212 and miR-483-5p at early time points (3 and 8 hours) (Figs 1 and 2A). [score:1]
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[+] score: 19
miR-132 and miR-212 have the same seed sequence and potential targets, although miR-132 is the preferentially expressed miRNA from the cluster (Lagos et al., 2010). [score:5]
Over -expression of miR-132 and miR-212 in HDLECs resulted in a drop in AGO2 mRNA (Fig. 1A). [score:3]
Similarly, in HDLECs the observed decrease in AGO2 mRNA levels following over -expression of the miR-132/miR-212 cluster (Fig. 1A) correlated with decreased AGO2 protein levels (Fig. 3A). [score:3]
We utilised a lentiviral construct containing the miR-132/miR-212 locus (Lagos et al., 2010) to screen for the effect of miR-132 on mRNA levels of 13 RBPs that were predicted miR-132 targets by multiple algorithms (Supplementary Table 2). [score:3]
2.3The miR-132/miR-212 cluster or AGO2-UTR were amplified from genomic DNA or cDNA respectively and subcloned into the pSIN lentiviral vector using the NotI and BamHI restriction enzymes. [score:1]
The miR-132/miR-212 cluster or AGO2-UTR were amplified from genomic DNA or cDNA respectively and subcloned into the pSIN lentiviral vector using the NotI and BamHI restriction enzymes. [score:1]
The effect was abolished when using a construct where the seed sequence of both miR-132 and miR-212 is mutated (Fig. 1A). [score:1]
The transcription of miR-132/miR-212 cluster is dependent on cAMP response element -binding (CREB) protein phosphorylation (Vo et al., 2005), which is inducible in an ERK-1/2 and MSK-1/2 dependent manner (Remenyi et al., 2010). [score:1]
Lymphatic endothelial cells microRNA RNA -binding proteins AGO2 miR-132 The mature miR-132 (miR-132-3p) is derived from the primary miR-132/miR-212 cluster, found in the intergenic region of chromosome 17p13.3. [score:1]
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[+] score: 19
We used miScript Primer Assays for 9 miRNAs (miR-744-5p, miR-648, miR-193b-3p, miR-212-3p, miR-143-3p, miR-93-5p, miR-222-3p, miR-423-3p and miR-766-3p) and QuantiTect Primer assays for 9 target genes (CDKN1A, MYC, PTEN, ESR1, ETS1, SOD2, MGMT, KRAS and HNF4A) (Qiagen, Hilden, Germany) to validate the different expression levels of the miRNA and their target genes, which are determined by miRTargetLink prediction software. [score:5]
Previous studies have identified that many miRNAs are expressed at low levels under normal condition and expressed strongly during pathological stress like miR-212, a cardiomyocyte-specific miRNA, which is strongly activated during heart failure. [score:5]
Out of the eight miRNAs, miR-648 was up-regulated and the seven remaining miRNAs were down regulated (miR-744-5p, miR-193b-3p, miR-212-3p, miR-143-3p, miR-93-5p, miR-423-3p and miR-766-3p). [score:5]
Several miRNAs were detected in cardiac tissue at different stages of development and are highly expressed in the fetal heart, including miR-212, miR-210 and miR-423 [41]. [score:4]
[1 to 20 of 4 sentences]
27
[+] score: 18
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-18a, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, hsa-mir-16-2, hsa-mir-196a-1, hsa-mir-198, hsa-mir-129-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-196a-2, hsa-mir-199b, hsa-mir-203a, hsa-mir-204, hsa-mir-210, hsa-mir-211, hsa-mir-181a-1, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-219a-1, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-224, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-137, hsa-mir-138-2, hsa-mir-140, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-127, hsa-mir-129-2, hsa-mir-138-1, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-320a, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-101-2, hsa-mir-219a-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-99b, hsa-mir-296, hsa-mir-130b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-365a, hsa-mir-365b, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-382, hsa-mir-383, hsa-mir-151a, hsa-mir-148b, hsa-mir-338, hsa-mir-133b, hsa-mir-325, hsa-mir-196b, hsa-mir-424, hsa-mir-20b, hsa-mir-429, hsa-mir-451a, hsa-mir-409, hsa-mir-412, hsa-mir-376b, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-181d, hsa-mir-499a, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-33b, hsa-mir-151b, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-301b, hsa-mir-216b, hsa-mir-103b-1, hsa-mir-103b-2, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-378b, hsa-mir-320e, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-219b, hsa-mir-203b, hsa-mir-451b, hsa-mir-499b, hsa-mir-378j
Gonadotropin-releasing hormone regulates multiple miRNA expression in gonadotrope cell lines, producing downregulation of miR-99b and miR-125b, and upregulation of miR-132, miR-151, miR-212, miR-222, miR-350, and miR-424 (Godoy et al. 2011). [score:10]
In Nile tilapia, the expression of miR-129-3p and miR-727-3p was significantly higher in mature females than males, whereas the expression of miR-132a and miR-212 was significantly higher in mature males than females (Xiao et al. 2014). [score:5]
Intronic miR-132 and miR-212 target p250RhoGAP, thereby guide morphological change and increase the motility of gonadotropes (Godoy et al. 2011). [score:3]
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28
[+] score: 16
In the present study, we also identified several microRNAs (e. g. miR-21-5p, miR-135b, miR-34a-5p, miR-212-3p, miR-302b-3p and miR-302c-3p) which proved by previous studies of heart disease with consistently aberrant expression in ARVC patients. [score:5]
Ahmetset al. have shown that miR-212 null mice could prevent the heart failure induced by pressure-overload, and directly target the FoxO3, an anti-hypertrophic and pro-autophagic transcription factor. [score:4]
Over expression of miR-212 was sufficient to induce hyper activation of pro-hypertrophic Calcineurin/NFAT signalling and impaired autophagy 49. [score:3]
A new miRNA-cross-talk including miR-212 and miR-30a-3p, through suppressing significant endothelial genes such as Grb2 associated binder 1 (GAB1) and Sirtuin 1(SIRT1) finally culminating in impaired endothelial function 33. [score:3]
The results showed that 11 of 12 significantly increased microRNAs had an optimal area value under the curve(AUC), among them, miR-1251, miR-21-3p, miR-21-5p, miR-212-3p and miR-34a-5p allowed for the discrimination between ARVC and healthy groups, corresponding to AUC of 0.978, 0.936, 0.944, 0.910 and 0.819 respectively ; however, miR-3674 was excluded for the AUC of it was 0.585 (Fig. 5). [score:1]
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29
[+] score: 15
miR-212 exerts a pro-apoptotic effect in lung cancer cells by targeting the anti-apoptotic gene PED, and inhibition of HDAC and the histone methyltransferase EZH2 strongly reactivates miR-212 expression in lung cancer cells. [score:7]
Epigenetic regulation of miR-212 expression in lung cancer. [score:4]
For example, downregulation of miR-212 in lung cancer cells is reportedly associated with H3K9me2 and H3K27me3 but not DNA hypermethylation (Incoronato et al., 2011; Figure 1). [score:4]
[1 to 20 of 3 sentences]
30
[+] score: 14
Disease Origin References of iPSC lines Phenotype of iPSC-derived neurons miRNAs of interest Fragile X syndrome Loss of function of FMRP (FMR1 gene) Urbach et al. (2010), Sheridan et al. (2011) Hyper-excitability of glutamatergic synapses DICER and AGO-1 complexes Rett’s syndrome Loss of function of MeCP2 transcriptional repressor Marchetto et al. (2010), Kim et al. (2011c), Cheung et al. (2012) Decreased soma size, neurite atrophy, decreased efficiency of glutamatergic synapses miR-132, miR-184, miR-483-5p, miR-212 Schizophrenia Multifactorial Urbach et al. (2010); Brennand et al. (2011), Paulsen Bda et al. (2012), Robicsek et al. (2013) Diminished neuronal connectivity miR-17-5p, miR-34a, miR-107, miR-122, miR-132, miR-134, miR-137 Down’s syndrome Additional copy of chromosome 21 Briggs et al. (2013), Weick et al. (2013) Reduced synaptic activity, increased sensitivity to oxidative stress miR-99a, miR-125b, miR-155, miR-802, Ret 7c Micro -RNAs, as fine regulators of protein translation, influence directly the level of gene expression. [score:9]
MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212. [score:3]
Disruption of MeCP2 gene in mice leads to the dysregulation of a set of miRNA potentially of influence in neurogenesis including miR-132, miR-184, miR-483-5p, and miR-212 (Nomura et al., 2008; Im et al., 2010; Urdinguio et al., 2010; Han et al., 2013). [score:2]
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31
[+] score: 14
After determining the expression levels of these miRNAs in the same 7 pairs of NSCLC tissues and normal adjacent tissues, we observed that 8 miRNAs (miR-203, miR-30, let-7, miR-132, miR-181, miR-212, miR-101 and miR-9) were downregulated in the NSCLC tissues, while the other 5 miRNAs (miR-125, miR-98, miR-196, miR-23 and miR-499) were upregulated (Fig. S1). [score:9]
In addition to let-7, miR-181 26, miR-30 29, miR-9 27 28, miR-132 32 33, miR-101 30 and miR-212 31 have also been shown to directly bind the 3′-UTR of LIN28B and repress the translation of this protein. [score:4]
A total of 13 miRNAs, including miR-203, miR-30, let-7, miR-132, miR-181, miR-212, miR-101, miR-9, miR-125, miR-98, miR-196, miR-23 and miR-499, were identified as candidate miRNAs by all three computational algorithms (Table S2). [score:1]
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32
[+] score: 13
92) 43 hsa-mir-302a dbDEMC 19 hsa-let-7g dbDEMC, miR2Disease 44 hsa-mir-212 literature 20 hsa-let-7b dbDEMC, HMDD, miR2Disease 45 hsa-mir-372 dbDEMC 21 hsa-mir-150 dbDEMC, literature 46 hsa-mir-197 dbDEMC 22 hsa-mir-338 dbDEMC 47 hsa-mir-124 literature 23 hsa-mir-103 dbDEMC, miR2Disease 48 hsa-mir-378 HMDD 24 hsa-mir-15b dbDEMC, HMDD 49 hsa-mir-26b dbDEMC, miR2Disease 25 hsa-mir-31 dbDEMC, HMDD, miR2Disease 50 hsa-mir-542 higher RWRMDA (No. [score:11]
Pathol Oncol Res Mar 3. 42 Ramalinga M, Srivastava A, Dimtchev A, Soldin O, Li J, et al (2012) MicroRNA-212 targets multiple signaling pathways in prostate cancer. [score:2]
[1 to 20 of 2 sentences]
33
[+] score: 13
Eight up-regulated miRNAs, including miR-19a-3p, miR-877-3p, miR-148a-3p, miR-212-5p, miR-1825, miR-210-3p, miR-940, and miR-134-5p, and two down-regulated miRNAs, miR-3609 and miR-145-5p, were identified as statistically significant different miRNAs. [score:7]
For example, miR-212 was down-regulated in ovarian cancer, potentially due to the significant enrichment of EZH2 and H3K27me3 in the promoter region[18]. [score:4]
No studies on the relationship between the other miRNAs, miR-877-3p, miR-212-5p, miR-1825, miR-940, miR-134-5p, and miR-3609, and PE have been reported. [score:1]
Considering that the conversion of the biological functions of normal cells is fundamental to the pathology of PE and carcinoma, we infer that miR-877-3p, miR-212-5p, miR-1825, miR-940, miR-134-5p, and miR-3609 might take part in the progression of PE. [score:1]
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34
[+] score: 13
There are also a number of miRNAs such as miR-132, miR-212, miR-130a and miR-152 shown to be upregulated in the pancreatic islets of the wi dely-studied T2D mo del Goto-Kakizaki rats (Esguerra et al., 2011) with active roles in beta cell stimulus-secretion coupling (Malm et al., 2016; Ofori et al., 2017). [score:4]
miR-132 and miR-212 expression in INS-1 832/13 cells (A–B) or in EndoC-βH1 cells (C–D) at different confluences. [score:3]
Among the other miRNAs included in this study, we observed significantly higher expression levels of miR-132 and miR-212 at higher confluences in INS-1 832/13 cells (Figs. 3A– 3B) but only an increasing trend in the human EndoC-βH1 cells (Figs. 3C– 3D). [score:3]
The following primers from TaqMan [®] Gene Expression and TaqMan [®] miRNA Assays were used for qPCR: Cav1/CAV1 (Rn00755834_m1/Hs00971716_m1), Aifm1/AIFM1 (Rn00442540_m1/ Hs00377585_m1), miR-375 (TM_ 000564), miR-200a (TM_000502), miR-130a (TM_00454), miR-152 (TM_000475), miR-132 (TM_000457) and miR-212 (TM_002551) were used for qPCR. [score:1]
We also investigated the influence of confluence on the expression levels of miR-200a, miR-130a, miR-152, miR-132 and miR-212. [score:1]
Although we showed that miR-375, which is one of the most enriched beta cell miRNA was not significantly influenced by confluence level in cultured rat and human beta cell lines, we clearly demonstrated that miR-132 and miR-212 are more dependent on cellular densities, as was shown for some miRNAs in other cells types (Hwang, Wentzel & Men dell, 2009; Van Rooij, 2011). [score:1]
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[+] score: 13
Two other miRNAs found in this study to be downregulated by exposure to the HNSCC patient serum, namely miR-212-5p and miR-132-5p, also target proteins involved in cell cycle regulation. [score:7]
MiR-212-5p targets CCND1 and miR-132-5p targets Bcl2. [score:5]
MiR-132 and miR-212 are formed by differential processing of the same primary miRNA. [score:1]
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36
[+] score: 12
Nevertheless, no decrease of the reporter gene was observed when miR-212 was co -transfected with the parts #1, #2, #3, nor #4. These results demonstrated that miR31, miR-708, and miR34c, but not miR-212, were able to target NOS1-3′UTR sequences leading to a decrease of the reporter gene Firefly luciferase expression. [score:5]
Furthermore, by analyzing the sequence of the NOS1-3′UTR regarding the 4 selected miRNAs, we identified 5 sequences as potential targets of miR-31, 5 for miR-708, 9 for miR-34c, and 3 for miR-212 (Additional file  3: Table S1 and Fig.   3a). [score:3]
A higher level of expression of the 4 miRNAs was detected in BMDd45-55 compared to control muscles with a fold change of 6.6, 4.4, 10.1, and 3.3 for miR-31, miR-708, miR-34c, and miR-212, respectively, confirming the results obtained by TLDA (Fig.   2b, Additional file  2). [score:2]
We selected 4 miRNAs (i. e., miR-31, miR-708, miR-34c, and miR-212) since they were overexpressed in muscular biopsies of BMDd45-55 patients compared to healthy subjects or in muscular biopsies of patients with severe phenotypes compared to other patients. [score:1]
Each 3′UTR construction (24.5 ng) was co -transfected in 293T-HEK cells with 25 pg of either miR -negative control (AM17111, Ambion) or miR-212, miR-31, miR-34c, or miR-708 (AM17100, Ambion) using lipofectamine 2000 diluted in Optimem reduced medium. [score:1]
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37
[+] score: 12
Clinical and preclinical studies have shown that miRNA-212 is up-regulated during heart failure [45, 83, 84]. [score:4]
These studies indicate that miRNAs, miRNA-208, miRNA-23a, miRNA-24, miRNA-125, miRNA-21, miRNA-129, miRNA-195, miRNA-199, and miRNA-212 are frequently increased in response to cardiac hypertrophy, whereas, miRNA-29, miRNA-1, miRNA-30, miRNA-133, and miRNA-150 expression are often found to be decreased. [score:3]
miRNA-212 targets Kir2.1 (KCNJ2 mRNA) that carries an inward rectifier K [+] current critical for maintaining membrane potential. [score:3]
Ucar A. Gupta S. K. Fiedler J. Erikci E. Kardasinski M. Batkai S. Dangwal S. Kumarswamy R. Bang C. Holzmann A. The miRNA-212/132 family regulates both cardiac hypertrophy and cardiomyocyte autophagy Nat. [score:2]
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[+] score: 12
In addition, miR-212 may function as a tumor suppressor through inhibition of the MYC and MECP2 potential target genes (2). [score:7]
As with miR-9, the downregulation of miRNA-212 has been reported to be partly associated with CGI hypermethylation, which is reversed by 5-aza-CdR treatment (2). [score:4]
miR-9 and miR-212. [score:1]
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39
[+] score: 12
Other miRNAs from this paper: mmu-mir-132, hsa-mir-132, mmu-mir-212
Note that the prediction tools (PITA, TargetScan, Pictar) made no distinction between miR-132 and miR-212 targets, as both miRs share the same seed sequence 20. [score:5]
Interestingly, Sirt1 mRNA levels (negatively) correlate with miR-212 in AD 62 (in contrast to our western blot data) and corroborates a multi-layered regulation of Sirt1 expression. [score:4]
Similar results were obtained with miR-212 (Fig. 2d,e). [score:1]
Notably, no correlation was found between miR-132 (or miR-212), Sirt1 and Aβ in individual groups (controls, MCI, AD) (see Supplementary Table S5). [score:1]
On the other hand, miR-212 did not correlate with Sirt1 (Fig. 4f). [score:1]
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40
[+] score: 11
We used a combination of two microRNA prediction methods, TargetScan and PicTar, to search for all predicted gene targets of the 5 most highly upregulated (let-7s, miR-21, miR-23b, miR-27a and miR-30a) and downregulated (miR-29b, miR-32, miR-144, miR-197 and miR-212) microRNAs [13]. [score:11]
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41
[+] score: 10
Pancreatic cancer-derived exosomes transfer miRNAs to dendritic cells and inhibit RFXAP expression via miR-212-3p. [score:5]
Ding et al. reported that exosomes derived from pancreatic cancer cells could deliver miR-212-3p to dendritic cells and inhibit RFXAP expression (Ding et al., 2015). [score:5]
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42
[+] score: 10
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-17, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-30a, hsa-mir-93, hsa-mir-96, hsa-mir-99a, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-105-1, hsa-mir-105-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-10a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-205, hsa-mir-181a-1, hsa-mir-222, hsa-mir-224, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-125b-1, hsa-mir-132, hsa-mir-141, hsa-mir-145, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, hsa-mir-150, hsa-mir-184, hsa-mir-188, hsa-mir-320a, hsa-mir-181b-2, hsa-mir-30c-1, hsa-mir-302a, hsa-mir-34c, hsa-mir-30e, hsa-mir-302b, hsa-mir-302c, hsa-mir-302d, hsa-mir-371a, hsa-mir-372, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-383, hsa-mir-339, hsa-mir-133b, hsa-mir-345, hsa-mir-425, hsa-mir-483, hsa-mir-146b, hsa-mir-202, hsa-mir-193b, hsa-mir-181d, hsa-mir-498, hsa-mir-518f, hsa-mir-518b, hsa-mir-520c, hsa-mir-518c, hsa-mir-518e, hsa-mir-518a-1, hsa-mir-518d, hsa-mir-518a-2, hsa-mir-503, hsa-mir-513a-1, hsa-mir-513a-2, hsa-mir-376a-2, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-645, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-744, hsa-mir-548e, hsa-mir-548j, hsa-mir-548k, hsa-mir-548l, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-302e, hsa-mir-302f, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-320d-1, hsa-mir-320c-2, hsa-mir-320d-2, hsa-mir-548q, hsa-mir-548s, hsa-mir-378b, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-548w, hsa-mir-320e, hsa-mir-548x, hsa-mir-378c, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, hsa-mir-371b, hsa-mir-548ao, hsa-mir-548ap, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, hsa-mir-548ay, hsa-mir-548az, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-548bc
Experiments with the bovine mo del showed that the expression of an oocyte-specific basic helix-loop-helix transcription factor FIGLA, essential for primordial follicle formation and expression of many genes required for fertilization and early embryonic survival, is regulated by miR-212 [37]. [score:6]
Using transient transfection and reporter assays, it turned out that miR-212 repressed the expression of FIGLA in bovine oocytes and embryos. [score:2]
MiR-212 was expressed in oocytes and increased in early embryos. [score:2]
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[+] score: 10
In breast cancer, miR-132, but not miR-212, inhibited cell proliferation and metastasis mediated by the NH1 gene (Hematological and Neurological expressed gene-1) (Zhang et al., 2014). [score:5]
Besides, inhibition of miR-212/132 in cells treated with TCDD and DIM mitigated the anti-invasive effects of these molecules, suggesting that miR-212/132 mediate, at least partially, the anti-metastatic effects of prototypical AhR ligands. [score:3]
The aryl hydrocarbon receptor/microRNA-212/132 axis in T cells regulates IL-10 production to maintain intestinal homeostasis. [score:2]
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44
[+] score: 10
Dou and his co-workers showed that miR-212 exerts its inhibitory effect on HCC by inhibiting FOXA1 expression via “seedless” 3’-UTR miRNA recognition elements [28]. [score:7]
Similar with miR-34a and miR-146b, miR-132 and miR-212, two tandemly expressed miRNAs, play vital roles in SIRT1-FOXO1 pathway. [score:3]
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45
[+] score: 10
In addition to let-7, the miRNAs miR-26a, miR-181, miR-9, miR-30, miR-125, miR-212 and miR-27 have also been shown to directly bind the 3′UTR of LIN28A/LIN28B and repress translation of the protein, and as these miRNAs are frequently under-expressed in malignant tumors, higher levels of LIN28 expression are seen [31– 34]. [score:8]
Notably, a potential regulatory loop reportedly exists between LIN28B and miR-212 in androgen-independent prostate cancer [35]. [score:2]
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46
[+] score: 9
The expression of miR-181c, miR-212 and miR-512 was silenced with DNA hypermethylation in gastric cancer, and their restored expression could induce decreased gastric cancer cell growth via inhibition of oncogenes expression (Refs 81, 82, 83). [score:9]
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47
[+] score: 9
Together, these data suggest that miR-212 directly targets Ptch-1 and increases cancer cell proliferation and invasion. [score:4]
Ma C miR-212 promotes pancreatic cancer cell growth and invasion by targeting the Hedgehog signaling pathway receptor patched-1J. [score:3]
Additionally, The level of miR-212 is also increased in PDAC tissues and cells, and luciferase assays demonstrated that PTCH1 is the target of miR-212 [57]. [score:2]
[1 to 20 of 3 sentences]
48
[+] score: 9
We previously demonstrated that miR-328 levels negatively correlated with BCRP mRNA and protein expression levels in the human placenta 7. In addition, we reported that the expression levels of miR-328 were regulated by an epigenetic mechanism 7. The methylation patterns of several CpG dinucleotides proximal to two C/EBPα -binding sites in the miR-328 5′-flanking region negatively correlated with miR-328 levels, and positively correlated with BCRP protein levels in human placental samples 7. Other miRNAs such as miR-519c, miR-520h, and miR-212 also regulate the expression of BCRP 28 29. [score:9]
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49
[+] score: 8
Using microarrays, we previously showed that 6 of 52 miRNAs were differentially expressed more than two fold in docetaxel-resistant SPC-A1/DTX cells compared with parental SPC-A1 cells, including three upregulated miRNAs (miR-192, miR-424 and miR-98) and three downregulated miRNAs (miR-200b, miR-194 and miR-212) [16]. [score:8]
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50
[+] score: 8
Experiments with monolayer cells and mice showed that exposure to alcohol increases miR-212 and hyperpermeability and downregulates zonula occludens-1 protein. [score:4]
Inhibition of miR-212 can reduce this effect; thus, this miRNA can be used as an interesting therapeutic intervention [106]. [score:3]
Tang Y. Zhang L. Forsyth C. B. Shaikh M. Song S. Keshavarzian A. The Role of miR-212 and iNOS in Alcohol-Induced Intestinal Barrier Dysfunction and Steatohepatitis Alcohol. [score:1]
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51
[+] score: 8
miR-19b-3p targets TIMELESS and NR1D2 and many of its correlated neighbours, let-7e-5p, miR-99b-5p and, indirectly, miR-140-3p (separated by 1 degree and connected via miR-214-3p and miR-212-3p) are instead down-regulated, suggesting a potential regulation of miR-19b-3p on these miRNAs. [score:8]
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[+] score: 8
miR-212 and miR-519e were also upregulated in the impaired monocyte but did not reach statistical significance (P = 0.09). [score:4]
Other miRNAs approaching significance with log2 fold changes up- or downregulation by greater than 1 included miR-10a, miR-133b, miR-138, miR-150, miR-155, miR-212, miR-362-3p, miR-518e, and miR-885-5p. [score:4]
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53
[+] score: 8
If we further apply the disease filter (selecting gastric cancer in the stomach), miR-212-3p is now hidden in only 22 predicted miRNA of MECP2. [score:3]
Even by considering the common predicted miRNAs from three existing miRNA target prediction databases (i. e. setting the database filter equal to three), miR-212-3p is still hidden in 537 predicted miRNAs of the gene MECP2, suggesting that applying the database filter alone is not an efficient way to reduce the non-functional miRNAs of MECP2. [score:3]
For example, human gene MECP2 is known to be regulated by miR-212-3p in gastric cancer cells [33]. [score:2]
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54
[+] score: 8
Later, it was shown that miR-212, located in the same cluster of miR-132, also targets MeCP2 and that MeCP2 silences the expression of both miRNAs, confirming the existence of a similar negative homeostatic feed-back loop between MeCP2 and mir-212, (Im et al., 2010). [score:5]
MeCP2 controls BDNF expression and cocaine intake through homeostatic interactions with microRNA-212. [score:3]
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55
[+] score: 8
Epigenetic regulation of miR-212 expression in lung cancer. [score:4]
Incoronato et al. showed that increases in H3K27me3 and H3K9me2 are observed in the mir-212 promoter region in the lung cancer cell line Calu-1, which has a low mir-212 expression level. [score:3]
In lung cancer, mir-212 is silenced by histone modifications rather than DNA methylation (Incoronato et al., 2011). [score:1]
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[+] score: 8
Only miR-212 was upregulated in human and downregulated in mouse PDAC samples. [score:7]
It is tempting to speculate that the discordance of miR-212 between human and mouse PDAC samples may indicate species differences of epithelial-stroma interactions during malignant progression [47]. [score:1]
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57
[+] score: 7
Overall, these results indicate that the altered expression of the miR-132/miR-212 family is dependent on mycobacterial virulence and, more specifically, that the presence of the virulence -associated RD1 locus is sufficient to account for the stronger induction of the miR-132/212 family among virulent mycobacteria. [score:3]
To quantify miRNA expression levels, cDNA was synthesized and quantitative real-time PCR (qPCR) performed using the Qiagen miScript PCR system and primers (miScript II RT Kit: 218161; miScript SYBR Green PCR kit: 218073; miR-92b-3p MS00032144; miR-132-3p MS00003458; miR-155–5p MS00031486; miR-212-3p MS00003815; miR-361-5p MS00004032; miR-361-3p MS00009555; U6 MS00033740) in a 7900 Real-time PCR system (Applied Biosystem). [score:2]
Additionally, both arms of miR-212—the other member of the miR-132/212 family due to their sequence homology and co-localisation on chromosome 17p13.3—also showed a vMTBC-specific response at 18h or 48h. [score:1]
Furthermore, infection with BCG::RD1 – a recombinant strain of BCG containing the RD1 locus, the absence of which accounts, to a large extent, for the attenuation of BCG [66] – significantly increased the induction of miR-132-3p and miR-212-3p, with respect to BCG, attaining a level that was not significantly different from cells infected with the virulent strains (Fig. 2C,D and S6 Table). [score:1]
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Similarly, CREB -induced miR-132 and miR-212, which share seed sequence homology, promote dendritic outgrowth from newborn neurons [55] and can target methyl CpG binding protein 2 (MeCP2), a regulator of neuroplasticity [56], [57]. [score:4]
miR-7, miR-124, miR-128, miR-132, and miR-212 are amongst the most highly down-regulated miRNAs found in glioblastomas compared to non-transformed cells (Fig. 1, Table S4, S6). [score:3]
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59
[+] score: 7
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-101-1, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-129-1, hsa-mir-148a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-210, hsa-mir-214, hsa-mir-215, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-129-2, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-130b, hsa-mir-376c, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-20b, hsa-mir-429, hsa-mir-449a, hsa-mir-433, hsa-mir-451a, hsa-mir-193b, hsa-mir-520d, hsa-mir-503, hsa-mir-92b, hsa-mir-610, hsa-mir-630, hsa-mir-650, hsa-mir-449b, hsa-mir-421, hsa-mir-449c, hsa-mir-378d-2, hsa-mir-744, hsa-mir-1207, hsa-mir-1266, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-4512, hsa-mir-378i, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j
Wada R. Akiyama Y. Hashimoto Y. Fukamachi H. Yuasa Y. miR-212 is downregulated and suppresses methyl-CpG -binding protein MeCP2 in human gastric cancer Int. [score:6]
In this context, it has been shown that oncomiR-10b, miR-21, and miR-212 in GC patients are associated with a high metastasis risk and poor clinical outcomes, including tumor-node-metastasis, tumor size, stage, lymph node metastasis, and five-year survival rate [69, 126, 228]. [score:1]
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60
[+] score: 7
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-211, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
A triple comparison was also done that included cbs [–/–], cbs [+/–] and STZ retinas, which revealed 6 miRNAs (miR-194, miR-16, miR-212, miR-30c, miR-5128 and miR-669c) that were commonly changed among cbs [–/–], cbs [+/–] and diabetes; 2 of these miRNAs were consistently changed among the three groups (miR-194 was upregulated and miR-16 was downregulated). [score:7]
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61
[+] score: 7
They have identified miR-483, miR-877, miR-337-5p, miR-546, and miR-494 as being upregulated, and miR-770-5p, miR-487b, miR-220, miR-212, and miR-712 as downregulated by adenosine signaling in MΦs. [score:7]
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62
[+] score: 7
Other miRNAs from this paper: hsa-mir-96
Previous profiling studies showed that miR-96 was downregulated and miR-212 was upregulated on PDAC tissues [24]. [score:7]
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63
[+] score: 7
Worth mentioning is the case of hsa-miR-132-3p and hsa-miR-212-3p that exhibit similar mature sequences and share the same seed region, yet only few targets were demonstrated to be targeted by both of them, and each of these miRNAs may also repress specific targets (Wanet et al. 2012). [score:7]
[1 to 20 of 1 sentences]
64
[+] score: 6
Various miRNAs, such as miR-200 (Yu et al., 2010), miR-146a (Li et al., 2010), miR-486 (Mees et al., 2009) and the let-7 family (Li et al., 2009b) have been confirmed to be tumor suppressors; meanwhile, pancreatic cancer malignancy was found positively associated with miR-196a (Huang et al., 2014), miR-212 (Ma et al., 2014) and miR-31 (Laurila et al., 2012). [score:3]
miR-212 promotes pancreatic cancer cell growth and invasion by targeting the hedgehog signaling pathway receptor patched-1. J. Exp. [score:3]
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65
[+] score: 6
Conversely, within the pro-myogenic pool, miR-424/-146b/-181a are associated with myogenesis and muscle development 28– 30. miR-212/-132 have been shown to inhibit MECP2 [31], which in turn regulates muscle maturation [32]. [score:5]
Following this RNA-seq -based filter, we identified miR-34c-5p/34c-3p/-362/-210/-590 for fibroblast-derived MiPs, and miR-212/-132/-424/-146b/-181a for MAB-MiPs (Fig.   4e and Supplementary Fig.   2). [score:1]
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66
[+] score: 6
Seven miRNAs (mmu-miR-574-5p, mmu-miR-466i-5p, mmu-miR-342-3p, mmu-let7i-5p, mmu-miR-34a-5p, mmu-miR-188-5p and mmu-miR-5119) were upregulated and the other five (mmu-miR-378a-3p, mmu-miR-202-3p, mmu-miR-378b, mmu-miR-378d and mmu-miR-212-3p) were downregulated in the CCl [4] group compared with the control (Fig. 1a,b). [score:6]
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67
[+] score: 6
Because of the prominence of the miRNA repression, we also wanted to verify the differential expression of a miRNA that was less strikingly down-regulated, such as miR-212-3p. [score:6]
[1 to 20 of 1 sentences]
68
[+] score: 6
On the contrary, the miRNAs up-regulated in FF, especially let-7b-5p, miR-15b-5p, miR-24-3p, miR-130b-3p, miR-146b-5p, miR-212-3p, miR-222-3p, miR-223-3p, miR-339-3p and miR-483-5p, with fold change values higher than 100-fold, could be transcribed in somatic follicular cells and move to oocytes by means of exosomes. [score:4]
Interestingly, let-7b-5p, miR-15b-5p, miR-24-3p, miR-130b-3p, miR-146b-5p, miR-212-3p, miR-222-3p, miR-223-3p, miR-339-3p and miR-483-5p showed expression fold changes higher than 100-fold (ln RQ > 4.7) compared to oocytes (Figure 3B and Supplementary Table S1). [score:2]
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69
[+] score: 6
miR-212 is shown to be strongly upregulated in pituitary tumours [176] and a study suggested death effector domain-containing protein (DEDD) as its potential target. [score:6]
[1 to 20 of 1 sentences]
70
[+] score: 6
Likewise, it was studied that aberrant expression of miR-212 in non-small cell lung cancer and in ovarian cancer cells induces apoptosis [36, 37]. [score:3]
For example, inhibition of miR-212 activates the apoptosis level in epithelial cells [33]. [score:3]
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71
[+] score: 6
Other miRNAs from this paper: hsa-mir-155
In particular, the microRNA miR-212 inhibits gene expression of zonula occludens gene (ZO-1), an important gene that regulates the formation of tight junctions in the gut lumen, especially in the colon (Tang et al. 2008). [score:6]
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72
[+] score: 6
Nine miRNAs (miR-519a, miR-212, miR-320b, miR-27a [∗], miR-30d [∗], miR-23a [∗], miR-30d [∗], miR-23a [∗], and miR-10a [∗]) and 5 miRNAs (miR-375, miR-485-3p, miR-23b, miR-485-3p, miR-23b, miR-627, and miR-1197) were up- or downregulated by glucose, respectively (Figure 2). [score:4]
miR-375 and miR-212 had been previously identified as regulated by glucose in rat islets [21]. [score:2]
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73
[+] score: 6
The expression pattern of 12 specific upregulated miRNAs (miR-17-3p, miR-21, miR-106a, miR-146, miR-155, miR-191, miR-192, miR-203, miR-205, miR-210, miR-212, miR-214) in tumor samples was similar in the tumor plasma-derived exosomes and distinct from the control samples, indicating exosomal miRNAs could be relevant as a screening method for this tumor (122). [score:6]
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74
[+] score: 5
Other miRNAs from this paper: hsa-mir-15a, hsa-mir-16-1, hsa-mir-30d
Luo X-J MicroRNA-212 Inhibits Osteosarcoma Cells Proliferation and Invasion by Down-Regulation of Sox4Cell. [score:5]
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75
[+] score: 5
The miRNA expression databases further show that miR-214-3p, miR-212-5p, miR-204-3p, miR-362-3p, miR-450a and miR-320 are expressed in the brain. [score:5]
[1 to 20 of 1 sentences]
76
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-29a, hsa-mir-33a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-134, mmu-mir-138-2, mmu-mir-145a, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, hsa-mir-192, mmu-mir-204, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-204, hsa-mir-211, hsa-mir-181a-1, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-134, hsa-mir-138-1, hsa-mir-206, mmu-mir-148a, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-330, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-212, mmu-mir-181a-1, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-106b, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-330, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-181d, hsa-mir-505, hsa-mir-590, hsa-mir-33b, hsa-mir-454, mmu-mir-505, mmu-mir-181d, mmu-mir-590, mmu-mir-1b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
MiR-132 and miR-212 are increased in pancreatic cancer and target the retinoblastoma tumor suppressor. [score:5]
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77
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In comparison, marginal comparisons validate an average of 7.83% of predicted targets, and yielded three miRNAs (miR-212, -29a and –29c) associated with significantly greater numbers of verifications than what might be expected under the no -targeting null with one additional miRNA (miR-133a) having a substantially greater number (p = 0.21). [score:5]
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78
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Tang Y. Banan A. Forsyth C. B. Fields J. Z. Lau C. K. Zhang L. J. Keshavarzian A. Effect of alcohol on miR-212 expression in intestinal epithelial cells and its potential role in alcoholic liver disease Alcohol. [score:5]
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79
[+] score: 5
In gastric carcinoma cells, microRNA miR-212 was shown to suppress translation of MECP2 transcripts, which in turn resulted in reduced depth of cellular invasion [124]. [score:5]
[1 to 20 of 1 sentences]
80
[+] score: 4
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-96, hsa-mir-100, hsa-mir-106a, hsa-mir-107, hsa-mir-192, hsa-mir-198, hsa-mir-129-1, hsa-mir-148a, hsa-mir-139, hsa-mir-10b, hsa-mir-34a, hsa-mir-182, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-214, hsa-mir-215, hsa-mir-216a, hsa-mir-217, hsa-mir-221, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-130a, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-129-2, hsa-mir-134, hsa-mir-146a, hsa-mir-149, hsa-mir-150, hsa-mir-154, hsa-mir-320a, hsa-mir-155, hsa-mir-128-2, hsa-mir-200a, hsa-mir-302a, hsa-mir-34b, hsa-mir-34c, hsa-mir-99b, hsa-mir-26a-2, hsa-mir-302c, hsa-mir-367, hsa-mir-370, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-379, hsa-mir-328, hsa-mir-151a, hsa-mir-135b, hsa-mir-335, hsa-mir-133b, hsa-mir-449a, hsa-mir-451a, hsa-mir-410, hsa-mir-486-1, hsa-mir-146b, hsa-mir-520f, hsa-mir-518d, hsa-mir-517c, hsa-mir-376a-2, hsa-mir-92b, hsa-mir-584, hsa-mir-602, hsa-mir-629, hsa-mir-638, hsa-mir-449b, hsa-mir-449c, hsa-mir-378d-2, hsa-mir-298, hsa-mir-1246, hsa-mir-1908, hsa-mir-718, hsa-mir-2861, hsa-mir-378b, hsa-mir-378c, hsa-mir-4306, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-3976, hsa-mir-4644, hsa-mir-203b, hsa-mir-451b, hsa-mir-4728, hsa-mir-4734, hsa-mir-378j, hsa-mir-6165, hsa-mir-486-2
Qu et al. (2009)MiR-203, MiR-212-3p Several proteins (attractin, complement proteins C3, C4 and C5, integrin, and lactotransferrin) The human pancreatic carcinoma epithelial like cell line PANC-1 cells Liquid chromatography-electro spray ionization mass spectrometry/mass spectrometry (LC-ESIMS/MS) analysis, Enzyme-linked immunosorbent assay (ELISA), and Western blotting The pancreatic cancer (PC)-derived exosomes down regulated the expression of TRL4 in dendritic cells (DCs) through miR-203, including immune tolerance. [score:3]
Cazzoli et al. (2013) MiR-17-3p, MiR-21, MiR-106a, MiR-146, MiR-155, MiR-191, MiR-192, MiR-203, MiR-205, MiR-210, MiR-212, and MiR-214 Plasma samples from patients with lung adenocarcinoma and a control group without known lung cancer or other active cancer Microarray analysis The considerable difference in total exosome and miRNA levels between lung cancer patients and controls, and the similarity between the circulating exosomal miRNA and the tumor-derived miRNA patterns, suggest that circulating exosomal miRNA might be useful as a screening test for lung adenocarcinoma. [score:1]
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81
[+] score: 4
Other miRNAs from this paper: hsa-mir-16-1, hsa-mir-16-2, hsa-mir-193a, hsa-mir-802
Moreover, miR-212 inhibits osteosarcoma cell proliferation and invasion by down -regulating Sox4 [22]. [score:4]
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82
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Five miRNAs have been extensively studied for their interaction with REST and their roles in promoting neurogenesis: miR-9 [9], [78], [79], miR-124 [9], [79], miR-132 [9], [79], [80], miR-135b [78] and miR-212 [80], many of which directly target neuronal genes. [score:4]
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83
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Serum was also analyzed by Q-RT-PCR for a panel of 20 tissue enriched and potential miRNA biomarkers, including those identified for liver (cfa-miR-122 and -885), heart/muscle (cfa-miR-1, -133, and -206), testis (miR-34b/c), pancreas (cfa-miR-216), brain (cfa-miR-212), and ubiquitously expressed cfa-miR-193b. [score:3]
A total of 22 miRNAs (Additional file 6: Figure S5) were selected for qPCR validation including the following 14 biomarker candidates of organ toxicity: liver (cfa-miR-122 and -885), pancreas (cfa-miR-216a/b); heart (cfa-miR-499); muscle (cfa-miR-206); heart/muscle (cfa-miR-1, -133a/b, and -208); testis (cfa-miR-34b/c); and brain and sciatic nervous tissues (cfa-miR-212, -432, and -885), and 5 miRNAs reported in the literature (cfa-miR-21, -192, -193a/b, and -200). [score:1]
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84
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On the contrary, we identified, among the upregulated miRNAs, members of the mir-132 and mir-212 families, that generated a specific cluster on chromosome 17. [score:4]
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85
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Other miRNAs were up-regulated: the five miRNAs with the largest increases were miR-9-5p, miR-192-5p, miR-193a-5p, miR-204-5p, and miR-212-3p. [score:4]
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86
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In the human study 10 miRNAs were extracted, and the change in their expression level varied significantly between F0 and F3 (F0 hsa-miR-146b, 199a, 199a*, 200a, 200b, 34a, and 34b, F0>F3: hsa-miR-212, 23b, and 422b). [score:3]
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87
[+] score: 3
In lung cancer, multiple miRNAs, such as let-7 family, miR-200, miR-486 and miR-146a have been identified as tumor suppressors [10– 14]; on the other hand, miR-31, miR-212 and miR-196a were found to promote NSCLC carcinogenesis [15– 17]. [score:3]
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88
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Dynamic expression of miR-132, miR-212, and miR-146 in the brain of different hosts infected with Angiostrongylus cantonensis. [score:3]
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89
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T mediated delivery of miR-212 down regulates PED (apoptosis related protein) and restore TRAIL (TNF-related apoptosis inducing ligand) mediated cytotoxicity in lung cancer [155]. [score:2]
Iaboni M Russo V Fontanella R Roscigno G Fiore D Donnarumma E Aptamer-miRNA-212 conjugate sensitizes NSCLC cells to TRAILMol Ther Nucleic Acids. [score:1]
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90
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In the first group, there were 19 miRNAs with an expression level that was four times higher in BCSCs than in MCF-7 cells: miR-122a, miR-152, miR-212, miR-224, miR-296, miR-31, miR-373*, miR-489, PRED_MIR127, PRED_MIR154, PRED_MIR157, PRED_MIR162, PRED_MIR165, PRED_MIR191, PRED_MIR207, PRED_MIR219, PRED_MIR246, PRED_MIR88 and PRED_MIR90. [score:3]
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91
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Ucar et al. [11] showed that the miRNA-212/132 family is indispensable during mice mammary gland development, particularly for the regulation of epithelial duct outgrowth. [score:3]
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92
[+] score: 3
List of the most highly expressed human microRNAs in salivary microvesicles are: hsa-let-7b, hsa-let-7c*, hsa-miR-128, hsa-miR-150*, hsa-miR-17, hsa-miR-1908, hsa-miR-212, hsa-miR-27b*, hsa-miR-29b, hsa-miR-29c, hsa-miR-335, hsa-miR-379*, hsa-miR-433, hsa-miR-454, hsa-miR-483-3p, hsa-miR-584, hsa-miR-621, hsa-miR-652, hsa-miR-760 and hsa-miR-888* [9]. [score:3]
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93
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We performed Assay 1 in 293T cells using hundreds of miRNA minigenes in our genetic library (Lu et al, 2011) and found that 4 miRNAs (miR-33a, miR-33b, miR-212 and miR-203) significantly down-regulated the c-Myc -dependent reporter (Fig 1B; Supporting Information Fig S1A). [score:3]
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94
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For example, knockdown of miRNA-212 prevented ethanol -induced disruption of the tight junction protein, zonula occludens-1 (ZO-1), in the intestinal epithelium of mice exposed to chronic alcohol [70]. [score:2]
Tang Y. Zhang L. Forsyth C. B. Shaikh M. Song S. Keshavarzian A. The Role of miR-212 and iNOS in Alcohol-Induced Intestinal Barrier Dysfunction and SteatohepatitisAlcohol. [score:1]
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95
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Verified gene targets of miR-187-3p, miR-486-5p, miR-34a, miR-212-3p, miR-34c-3p, miR-675-5p and miR-3911 were not enriched for GO terms related to cardiac and general toxicity responses. [score:3]
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96
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Regulation of TLR2 -mediated tolerance and cross-tolerance through IRAK4 modulation by miR-132 and miR-212. [score:2]
For example, miR-132 and miR-212-5p were specific to fungal exposure at 6 h time point, whereas miR-132, miR-212, and miR-129-5p were specific to fungal exposure at 12 h time point. [score:1]
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97
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yes white college students[67] colorectal cancer miR-337, miR-582, miR-200a-5p, miR-184, miR-212 CD86 rs17281995 G>C (for miR-337, miR-582, and miR-200a-5p, C impairs binding efficiency; for miR-184 and miR-212, C increases binding efficiency) in silico: miRNA target prediction program. [score:3]
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98
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Another example is miR-212, which has been involved in cetuximab-resistant cancer cells of head and neck carcinoma by directly regulating heparin -binding EGF-like growth factor (Hatakeyama et al, 2010). [score:3]
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99
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Interestingly, by stratifying patients according to survival status at five years, only two mature miRNAs (hsa-mir-499a-5p and hsa-mir-429) and one miRNA precursor (hsa-mir-212-prec) were found differentially expressed (Supplementary Table S1), being only mir-499a-5p in common with the MSC related signature. [score:3]
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100
[+] score: 2
Other miRNAs from this paper: hsa-mir-132, gga-mir-132a, gga-mir-132b, gga-mir-212, gga-mir-132c
Nahid MA, Yao B, Dominguez-Gutierrez PR, Kesavalu L, Satoh M, Chan EKL 2013 Regulation of TLR2 -mediated tolerance and cross-tolerance through IRAK4 modulation by miR-132 and miR-212. [score:2]
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