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67 publications mentioning rno-mir-200a

Open access articles that are associated with the species Rattus norvegicus and mention the gene name mir-200a. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 262
Other miRNAs from this paper: rno-mir-200c, rno-mir-200b
Downregulated miR-200a could Directly Target CTNNB1 and Activate the Wnt/β-catenin Pathway in WB Cells. [score:7]
By computational algorithms from TargetScan and mirBase target database, we found that the 3′-UTR of rat β-catenin (CTNNB1) mRNA contains a conserved putative miR-200a target site (Figure 4A). [score:7]
Thus, in addition to directly targeting CTNNB1 and regulating the Wnt/β-catenin pathway, there is a possibility that miR-200a may also exert its function on WB cells via targeting ZEB2. [score:7]
As shown in Figure 3C, consistent with their elongated mesenchymal morphology, down-regulated E-cadherin and up-regulated N-cadherin, as well as Vimentin, were detected in WB-anti-miR-200a cells. [score:7]
In addition, after miR-200a silencing in WB cells, mRNA expression of ZEB2, a well-acknowledged target of miR-200a, was constant (Figure 1C), whereas its protein expression increased (Figure 1D). [score:7]
Moreover, the expression of cyclin D1 and c-myc, two representative target genes of the Wnt/β-catenin pathway, was also enhanced following the knockdown of miR-200a in WB cells (Figure 4C). [score:6]
As shown in Figure 2E, expression of EpCAM, CD133, ABCG2, CK19 and AFP were much higher in WB-anti-miR-200a cells than in WB-miR-NC cells, whereas the ALB mRNA level was relatively downregulated, indicating that WB-anti-miR-200a cells are in a less differentiated state. [score:6]
Our results demonstrated that miR-200a expression was much higher in WB cells than in hepatoma cells (Figure 1A), indicating that down-regulated miR-200a may be associated with HCC malignant phenotypes. [score:6]
Third, WB-anti-miR-200a cells were in a less differentiated state by higher expression of primitive liver markers AFP and CK19, and lower expression of the mature liver marker ALB. [score:5]
Taken together, our data indicate that CTNNB1 mRNA is a direct target of miR-200a, and knockdown of miR-200a could activate, at least in part, the Wnt/β-catenin signaling pathway in WB cells. [score:5]
For β-catenin inhibition studies, transient transfection of WB-anti-miR-200a cells with small-interfering RNA (siRNA) targeting CTNNB1 mRNA (siCTTNB1, Santa Cruz Biotechnology) or control siRNA (siControl, Santa Cruz Biotechnology) was performed. [score:5]
Second, putative hepatic CSC markers (EpCAM [30], CD133 [8] and ABCG2 [39]) were up-regulated after miR-200a knockdown. [score:5]
To conclude, our data suggested that downregulation of miR-200a in liver oval cells promotes EMT and CSC-like traits in vitro, partially through the regulation of β-catenin signaling, and finally give rise to tumorigenicity in vivo. [score:5]
In our study, WB cells stably lacking miR-200a also presented mesenchymal characteristics, including elongated cell morphology, enhanced cell migration ability, down-regulated E-cadherin and up-regulated N-cadherin, as well as Vimentin. [score:5]
Regarding the molecular mechanisms underlying the role of miR-200a in WB cells, we used combined bioinformatics and experimental approaches to identify CTNNB1 as a direct functional downstream target of miR-200a. [score:4]
Downregulation of miR-200a confers tumorigenicity to WB cells in vivo. [score:4]
Expression Levels of miR-200a and Validation for Stable miR-200a Knockdown in WB Cells. [score:4]
In previous studies, miR-200a regulating the EMT process by targeting EMT-activating transcriptional factors ZEB1 and ZEB2 has been thoroughly elaborated in different types of cancers [55], [56]. [score:4]
As an important regulatory factor, the miR-200 family has been identified as suppressors of CSC-like or EMT-like phenotypes and functions in various normal and cancer cells [22], [23], [24], [36]. [score:4]
Downregulation of miR-200a Confers Tumorigenicity to WB Cells in vivo. [score:4]
QRT-PCR analysis showed the expression level of miR-200a in WB-anti-miR-200a cells decreased compared with WB-miR-NC cells, whereas its level was constant in WB-miR-NC cells versus WB cells (Figure 1B), suggesting that lentivirus infection was highly efficient and did not perturb endogenous miR-200a expression in WB cells. [score:4]
In addition to extensive participation in inhibiting epithelial mesenchymal transition (EMT) in various cancer cells [21], the miR-200 family is also inversely associated with regulating CSC phenotypes of breast cancer [22], [23], pancreatic cancer [24] and ovarian cancer [25]. [score:4]
miR-200a directly targets CTNNB1 and associates with Wnt/β-catenin pathway activity in WB cells. [score:4]
Expression levels of miR-200a and validation for stable miR-200a knockdown in WB cells. [score:4]
In our study, we also found knockdown of miR-200a led to overexpression of ZEB2 protein in WB cells. [score:4]
To conclude, the in vivo results indicated that downregulation of miR-200a in WB cells could induce tumorigenicity and finally give rise to tumors in nude mice. [score:4]
This is the first report, to the best of our knowledge, demonstrating that downregulation of miR-200a is associated with EMT and CSC-like phenotypes in HOCs. [score:4]
Interestingly, expression of the oncogene c-myc was also up-regulated in WB-anti-miR-200a cells (Figure 2E), suggesting that miR-200a silencing may also promote WB cells to obtain transformed characteristics. [score:4]
To validate predicted target genes, oligonucleotides (35 bp) containing wild-type or the mutated binding site for miR-200a from the rat β-catenin mRNA (CTNNB1) 3′-UTR were annealed and ligated into the EcoRI and PstI sites of the pGL3-control-mcs2 reporter vector (named pGL3-CTNNB1-wt or pGL3-CTNNB1-mut). [score:3]
Data are expressed as the mean ± SD (C) and representative dot plots of apoptosis tests are shown (D); n = 5. (E) Expression of EpCAM, CD133, ABCG2, CK19, AFP, ALB and c-myc in WB-anti-miR-200a cells measured by qRT-PCR. [score:3]
Furthermore, we identified β-catenin (CTNNB1) as the functional downstream target of miR-200a, and activation of the Wnt/β-catenin pathway is responsible, at least partially, for miR-200a-silencing -mediated biological functions in WB-F344 cells. [score:3]
More strikingly, miR-200 family members have been reported to be directly regulated by p53, further highlighting their role in tumor progression [46]. [score:3]
These results indicate that miR-200a is effectively and functionally suppressed in WB-anti-miR-200a cells, serving as the basis of the remaining experiments. [score:3]
Using loss-of-function studies, we demonstrated for the first time that suppression of miR-200a is associated with CSC-like features and the EMT phenotype in WB-F344 cells in vitro, and is responsible for the acquisition of tumorigenicity in vivo. [score:3]
As expected, the stimulatory effect of miR-200a-silencing on cyclin D1 and c-myc expression was abolished by siCTNNB1 transfection (Figure 5A). [score:3]
Our previous study also showed that miR-200a was greatly downregulated in the F344 rat HCC SP fraction cells compared with their normal counterparts [26]. [score:3]
As an initial step, the expression pattern of miR-200a was assessed in the WB-F344 cell line, BRL normal liver cell line and three other hepatoma cell lines (H-4-II-E, CBRH-7919, RH-35). [score:3]
We confirmed that transfection of siCTNNB1 did not induce a detectable miR-200a expression change in WB-anti-miR-200a cells (data not shown). [score:3]
To further elucidate whether elevated β-catenin expression and activated β-catenin pathway are functionally associated with miR-200a-silencing -mediated biological activities of WB cells, we used siCTNNB1 transfection and examined its effects on WB-anti-miR-200a cells. [score:3]
These findings underscore the importance of miR-200a in inhibiting neoplastic phenotypes in normal adult hepatic progenitor cells. [score:3]
Thus, we postulated that miR-200a might target genes associated with Wnt/β-catenin signaling. [score:3]
We provide evidence that miR-200a expression was relatively higher in WB cells and BRL cells than in three other rat hepatoma cell lines. [score:3]
Interestingly, using miRNA microarray and real-time quantitative polymerase chain reaction (qRT-PCR) analysis, our previous study showed that miR-200a was greatly downregulated in the F344 rat HCC side population (SP) fraction cells compared with their normal counterparts [26]. [score:3]
The immunofluorescence staining data illustrated that β-catenin expression showed strong cytoplasmic and some nuclear localization when miR-200a was silenced in WB cells (Figure 4D). [score:3]
As shown in Figure 4C, miR-200a silencing induced the protein expression of CTNNB1. [score:3]
0079409.g004 Figure 4 (A) Predicted alignment of miR-200a and a potential binding site at the 3′-UTR of rat CTNNB1 mRNA (624–630 nt) by TargetScan. [score:3]
We obtained evidence that miR-200a knockdown might also be associated with an EMT-like phenotype in WB cells. [score:2]
To this end, we hypothesized that miR-200a dysregulation might be implicated in the malignant transformation of hepatic stem cells. [score:2]
The results showed that anti-miR-200a transfection significantly increased the expression of luciferase containing a CTNNB1-wt 3′-UTR binding site for miR-200a in WB cells compared with the control (Figure 4B). [score:2]
Stable Knockdown of miR-200a Facilitates CSC-like Phenotypes in WB Cells. [score:2]
Moreover, except for EMT process and β-catenin pathway, miR-200a has also been found participating in epigenetic modulation through histone deacetylase 4/SP1/miR-200a regulatory network [38]. [score:2]
First, stable knockdown of miR-200a enhanced proliferation and conferred a greater potential for self renewal capacity even after serial passages in WB cells. [score:2]
miR-200a Target Luciferase Reporter Assay. [score:2]
The silencing of CTNNB1 and inhibition of β-catenin -mediated transcription activity in WB-anti-miR-200a cells were confirmed by western blot analysis (Figure 5A) and Top/Fop luciferase reporter assays (Figure 5B), respectively. [score:2]
Recently, it has been confirmed that the miR-200 family plays a key role in negatively regulating the EMT process [21]. [score:2]
Stable knockdown of miR-200a facilitates CSC-like phenotypes in WB cells. [score:2]
The function of miR-200a exerting on WB cells is indeed, at least in part, attributed to β-catenin regulation in Wnt/β-catenin signaling. [score:2]
Consistent with these theories, we demonstrated in this study that stable knockdown of miR-200a enhanced the β-catenin protein level. [score:2]
These results were also in line with previous studies reporting downregulation of miR-200a in poorly differentiated HCC cell lines compared with well differentiated cell lines and in HCC tissues compared with the adjacent noncancerous hepatic tissues [37], [38]. [score:2]
To further validate the function of siCTNNB1 on β-catenin -mediated transcription activity, WB-anti-miR-200a cells were co -transfected with TopFlash or FopFlash and siCTNNB1 using Lipofectamine 2000 (Invitrogen) in the same way. [score:1]
Number of spheroids formed in the primary, secondary and tertiary generations of suspension cultured WB-miR-NC or WB-anti-miR-200a cells (right). [score:1]
Single-cell suspensions of WB-miR-NC or WB-anti-miR-200a cells were plated at a density of 1×10 [6] cells per well in 6-well Ultra-Low Attachment Plates (Corning) and maintained in serum-free medium for 7 days. [score:1]
WB-miR-NC or WB-anti-miR-200a cells were seeded in a 24-well plate (Corning, Lowell, MA) at 1×10 [4/]well in triplicate and maintained under standardized culture conditions. [score:1]
For C, data are normalized to β-actin and presented as the mean ± SD; n = 4. Next, we established lentivirus -mediated stable WB-anti-miR-200a and WB-miR-NC cell lines. [score:1]
0079409.g006 Figure 6 (A) Subcutaneous tumors developed by WB-miR-NC or WB-anti-miR-200a for 40 days post inoculation (left). [score:1]
To further determine the characteristics of WB-anti-miR-200a cells, expression of putative hepatic CSC markers were examined by qRT-PCR. [score:1]
WB cells were lentivirally transfected with either the GV232-Puro-anti-miR-200a recombined vector (WB-anti-miR-200a) or empty GV232-Puro vector (negative control, WB-miR-NC). [score:1]
Based on these morphologic changes as well as biological and biochemical behaviors shown in WB-anti-miR-200a cells, we conclude that miR-200a silencing induces the EMT-like phenotype in WB cells. [score:1]
By assessing the apoptotic cells after exposure to anticancer drugs, we showed that WB-anti-miR-200a cells exhibited reduced apoptosis upon paclitaxel or doxorubicin (15.1±2.1% or 11.2±1.9%, respectively) treatment, in contrast to WB-miR-NC cells (25.8±3.4% or 18.3±2.7%, respectively) (Figure 2F), indicating that WB-anti-miR-200a cells might be more resistant to anticancer drugs. [score:1]
The miR-200 family is a group of evolutionarily conserved miRNAs, comprising five members (miR-200a, -200b, -200c, -141 and -429). [score:1]
Lentivirus -mediated silencing of miR-200a was verified by qRT-PCR and western blot analysis. [score:1]
WB-miR-NC or WB-anti-miR-200a cells were resuspended in serum-free medium, and then 200 µl of the single-cell suspension (2×10 [4] cells) was seeded onto the upper chamber of each transwell. [score:1]
Morphologically, WB-anti-miR-200a cells were partly spindle shaped similar to mesenchymal cells, whereas WB-miR-NC cells were tightly bound, oval-like cells with an epithelial phenotype (Figure 3A). [score:1]
In addition, the differences in cell proliferation and spheroid forming ability were not due to differences in apoptosis, because caspase-3/7 activity and the ratio of apoptotic cells were similar between miR-200a silencing cells and control cells (Figure 2C and 2D). [score:1]
Functional studies showed that WB cells stably lacking miR-200a exhibited CSC-like properties. [score:1]
Exploring miR-200a -based prevention and therapeutics might benefit HCC clinically. [score:1]
For C, data are normalized to β-actin and presented as the mean ± SD; n = 4. Next, we established lentivirus -mediated stable WB-anti-miR-200a and WB-miR-NC cell lines. [score:1]
To validate the prediction, a 3′-UTR fragment of rat CTNNB1 mRNA containing wild-type or a mutated binding site for miR-200a was cloned into a luciferase reporter vector. [score:1]
Furthermore, we observed dramatic diminished spheroid formation (Figure 5C) and reduced migration abilities (Figure 5D) following CTNNB1 silencing in WB-anti-miR-200a cells. [score:1]
As shown in Figure 6A, WB-anti-miR-200a cells developed visible tumors on every right flank of the five nude mice, whereas no exhibited tumor was observed on the left flanks injected with WB-miR-NC cells. [score:1]
Briefly, WB-miR-NC or WB-anti-miR-200a cells were plated at 1×10 [4/]well into clear, opaque-wall 96-well plates (Corning) and incubated for 24 h. After the medium was removed, Caspase-Glo 3/7 reagent (100 µl) was added, gently mixed, and incubated at room temperature for 30 min. [score:1]
As in vitro studies showed that stable knockdown of miR-200a facilitates CSC-like signatures and EMT phenotypes in WB cells, we performed xenograft formation assay to further investigate the tumorigenicity mediated by miR-200a suppression. [score:1]
To investigate the possible role of miR-200a on OCs, we first performed qRT-PCR to analyze the expression levels of miR-200a in WB cells as well as in BRL normal rat liver cells and three hepatoma cell lines (H-4-II-E, CBRH-7919, RH-35). [score:1]
As a result, we introduced miR-200a loss-of-function studies in WB cells in the following research. [score:1]
The Anti-miR-200a Effects can be Partially Attenuated by Silencing of CTNNB1 in WB-anti-miR-200a Cells. [score:1]
Moreover, we also performed western blot analysis to detect β-catenin protein levels in WB-anti-miR-200a cells and WB-miR-NC cells. [score:1]
WB-miR-NC or WB-anti-miR-200a cells were cultured in 6-well plates (Corning) at 1×10 [5] cells per well and were then treated with paclitaxel (10 ng/mL) or doxorubicin (30 ng/mL), respectively. [score:1]
However, the function miR-200a exerts on hepatic stem cells and hepatic CSCs is rarely reported. [score:1]
Consistent with their findings, a rescue experiment in our study found WB-anti-miR-200a transduced with siCTNNB1, but not scrambled siControl, showing diminished spheroid formation and reduced migration ability in vitro. [score:1]
WB-miR-NC or WB-anti-miR-200a cells were mixed with Matrigel Basement Membrane Matrix (BD Biosciences) at ratio of 1∶1 and then subcutaneously implanted into left flanks (WB-miR-NC) or right flanks (WB-anti-miR-200a) of five nude mice at 2×10 [6] cells per injection, respectively. [score:1]
Next, using a lentiviral vectors approach, we transfected WB cells with miR-200a antagomirs and stably silenced miR-200a in WB cells, results that were confirmed by qRT-PCR and western blotting. [score:1]
WB cells were co -transfected with the above recombinant plasmids and 50 nM anti-miR-200a or anti-miR-control (Ambion, Austin, TX) using Lipofectamine 2000 (Invitrogen). [score:1]
Expression levels of rno-miR-200a were quantified using a miScript PCR System (QIAGEN, Hilden, Germany), including a miScript II RT Kit, miScript Primer Assays and miScript SYBR Green PCR Kit. [score:1]
Collectively, these results demonstrate that activation of the Wnt/β-catenin pathway is functionally relevant to miR-200a-silencing -mediated biological activities of WB cells. [score:1]
To assess β-catenin -mediated transcription activity in WB-anti-miR-200a cells, we employed the Top/Fop reporter gene system as previously described [29]. [score:1]
WB cells were co -transfected with anti-miR-200a (or anti-miR-control) and the pGL3-CTNNB1-wt (or pGL3-CTNNB1-mut) vector. [score:1]
Fourth, miR-200a silencing led to superior anti-apoptosis capacity to chemotherapeutic drugs in WB cells. [score:1]
0079409.g003 Figure 3 (A) Morphological changes in WB-miR-NC and WB-anti-miR-200a cells (magnification×200). [score:1]
The anti-miR-200a effects are partially attenuated by silencing of CTNNB1 in WB-anti-miR-200a cells. [score:1]
Briefly, the WB-miR-NC or WB-anti-miR-200a cells were collected, washed in cold PBS, incubated for 15 min with Annexin V-FITC and PI according to the manufacturer’s protocol, and then analyzed by a FACSCalibur flow cytometer and CellQuest software (BD Biosciences, San Jose, CA). [score:1]
Our finding is in accordance with phenomena previously observed in pancreatic cells [47] and nasopharyngeal carcinoma cells [48], indicating that miR-200a indeed plays an extensive and profound role in the context of cancer initiation and progression. [score:1]
0079409.g002 Figure 2 (A) Growth curve of WB-miR-NC and WB-anti-miR-200a cells determined by cell counting. [score:1]
[1 to 20 of 102 sentences]
[+] score: 184
Other miRNAs from this paper: rno-mir-200c, rno-mir-200b
Our study identified β-catenin as a direct target of miRNA-200a, suggesting that miRNA-200a exerts its anti-fibrotic effects via directly down-regulated β-catenin expression. [score:10]
Using miR-200a mimics to transfect HSC, we found that the expression of p-STAT3 was increased in HSC with the overexpression of miR-200a, which was contrast to the expression of β-catenin, and transfection of miR-200a inhibitors in HSC resulted in decreased of p-STAT3 and increased of β-catenin (Fig. 8B). [score:9]
A recent study showed that miRNA-200a silencing activated HSC through Keap1, while overexpression of miRNA-200a inhibited HSC proliferation 8. Consistent with Yang et al. 8 study, we found that expression of miRNA-200a was reduced in the activated HSC as well as in fibrotic rat liver tissues compared with controls, suggesting that loss of miRNA-200a induces development of liver fibrosis. [score:7]
Primary HSC cells pre-incubated with TGF-β1 for 24 h and subsequently cultured with 1.5 ng/mL IL-22 for 48 h. For activated HSC cells, treatment with IL-22 significantly inhibited HSC proliferation (Fig. 5A) and suppressed mRNA levels of α-SMA and Col I in the supernatant (Fig. 5B,C), Of note, treatment with IL-22 induced mRNA expression of miR-200a (Fig. 5D) and decreased mRNA and protein levels of β-catenin in the activated HSC cells (Fig. 5E–G). [score:7]
To overexpress and knock down miR-200a, lentiviruses of rno-miR-200a mimics, miR-200a inhibitors and a non-specific control were transduced into HSC cells (Genepharma, Shanghai, China). [score:6]
The expression levels of miR-200a in rat fibrotic liver significantly decreased in the group treated with miR-200a inhibitor injection compared with PBS group and IL-22 + miR-200a inhibtors group (Fig. 7A). [score:6]
Similar to the results of expression of miR-200a, we found that the liver fibrosis recovery slower after miR-200a inhibitor injection compared with PBS group and the IL-22 + miR-200a inhibitor group according to the Ishak fibrosis score (Fig. 7B). [score:6]
Target prediction for miR-200a suggested that it regulates the expression of β-catenin through a potential seed region in 3′UTR (Fig. 4A). [score:6]
To confirm that β-catenin is a direct target of miR-200a, we obtained luciferase-3′UTR reporter constructs for the mRNA and transfected them into HEK293T cells together with miR-200a mimics or a non -targeting control miRNA. [score:6]
We also observed that the expression of p-STAT3 was increased in the group of miR-200a inhibitor injection compared with PBS group and IL-22 + miR-200a inhibitors group (Fig. 7C,D). [score:6]
To knock down the expression of miR-200a, rats with liver fibrosis (n = 10) were hydrodynamicaly tail vein injected with lent-miR-200a inhibitors (1 × 10 [8] TU/mL) in PBS for 1 week. [score:6]
We found that overexpression of miR-200a inhibited not only HSC-T6 but also primary HSC proliferation (Fig. 3A). [score:5]
HSC-T6 and primary HSC were activated by incubation with 5 ng/mL TGF-β1 for 48 h. After HSC activation, expression of miR-200a remarkably decreased (Fig. 2A), while expression of β-catenin significantly increased in mRNA (Fig. 2B) and protein levels (Fig. 2C,D). [score:5]
The relative gene expression was normalized to the level of GAPDH while expression of miR-200a was normalized to the level of U6. [score:5]
Since HSC activation suppressed expression of miR-200a, we further overexpressed miR-200a with a lentiviral vector in HSC and measured its effect on proliferation and apoptosis. [score:5]
Moreover, IL-22 treatment induced expression levels of miR-200a (Fig. 6B) and reduced mRNA and protein expression of β-catenin in rat fibrotic liver compared with controls (Fig. 6C,D). [score:4]
Overexpression and knock down miR-200a in HSC. [score:4]
Taken together, these results indicated that IL-22 inhibited HSC activity through the regulation of miR-200a/β-catenin. [score:4]
In conclusion, our results demonstrate that IL-22/STAT3 regulates HSC activation and ameliorates liver fibrosis through modulating expression of miR-200a and β-catenin. [score:4]
IL-22 inhibited HSC activity via regulation of miR-200a. [score:4]
In order to explore the relationship between IL-22 and miR-200a in HSC activity, we knocked down miR-200a in HSC cells using its inhibitors, subsequently treated cells with IL-22 protein and measured cell proliferation, mRNA and protein expression. [score:4]
IL-22 inhibited HSC activation via regulation of miR-200a/β-catenin. [score:4]
The proliferation of HSC was increased and then compared to that without miR-200a inhibitors transfection (Fig. 5H), and the expression of β-catenin increased significantly (Fig. 5I–K). [score:4]
miR-200a inhibited HSC proliferation. [score:3]
After transduction with rno-miR-200a lentivirus for 72 h, cells were monitored under immunofluorescence microscopy to ensure at least 80% of the cells expressed green fluorescence protein (GFP). [score:3]
miR-200a targeting β-catenin in HSC. [score:3]
The constructs were transfected into HEK293 cells together with miR-200a or miR-200a inhibitors by using Lipofectamine 2000 (Invitrogen). [score:3]
Expression of miR-200a and β-catenin was decreased during HSC activation. [score:3]
IL-22 alleviated liver fibrosis and increased miR-200a expression in rat. [score:3]
Our study showed treatment with IL-22 induced the expression of miR-200a, decreased β-catenin in HSC and rat fibrotic liver tissues via STAT3 pathway. [score:3]
3′UTR mutagenesis of sequence complementary to the miR-200a seed region attenuated miRNA effect (Fig. 4C,D), suggesting that β-catenin is a directly regulated by miR-200a in HSC. [score:3]
qRT-PCR was used to detect the expression of miR-200a. [score:3]
β-catenin was a downstream target of miR-200a. [score:3]
The sequences were as follows: miRNA-200a mimic sense 5′-UAA CAC UGU CUG GUA ACG AUG U-3′ and anti-sense 5′-ACA UCG UUA CC A GAC AGU GUU A-3′, and miRNA-200a inhibitor sequences were 5′-ACA UCG UUA CCA GAC AGU GUU A-3′. [score:3]
Effect of IL-22 on liver fibrosis was reduced by miR-200a inhibitor transfection. [score:3]
Expression of miR-200a and β-catenin after HSC activation. [score:3]
Collectively, these results suggested an inhibitory role of miR-200a in HSC proliferation. [score:3]
miR-200a inhibited proliferation of HSC. [score:3]
β-catenin and STAT3 protein expression in response to miR-200a in HSC. [score:3]
Collectively, these results suggested that miR-200a was involved in the regulatory function of IL-22 in alleviating liver fibrosis. [score:2]
Knocking-down miR-200a. [score:2]
The miRNA-200 family was reported to be an important one in liver fibrogenesis 19 20. [score:1]
The sequences of β-catenin 3′-UTR containing the predicted miR-200a binding sites were cloned into psiCHECK2 (C8021, Promega, USA). [score:1]
, Minneapolis, USA) for 48 h for activation 11. miR-200a was isolated from cells or homogenized liver tissues using miRVana miRNA isolation kit (Takara, Dalian, China). [score:1]
To further elucidate the relationship between IL-22 and miR-200a in liver fibrosis, a fibrotic rat mo del was IP injected with rrIL-22. [score:1]
How to cite this article: Hu, B. et al. Interleukin-22 ameliorates liver fibrosis through miR-200a/beta-catenin. [score:1]
[1 to 20 of 46 sentences]
[+] score: 181
revealed negative expression correlation between miR-200 family and their target genesTo study how miR-200 family contributed to epididymal region-specific gene expression, we performed to examine whether putative target genes of miR-200 family were coordinately more or less expressed between caput and cauda epididymis. [score:11]
Given the higher expression of miR-200 family in the caput region, it was suggested that differentially expressed miR-200 family down-regulated their target genes in the epididymis. [score:10]
To study how miR-200 family contributed to epididymal region-specific gene expression, we performed to examine whether putative target genes of miR-200 family were coordinately more or less expressed between caput and cauda epididymis. [score:7]
The temporal and spatial manners of miR-200 family expression may contribute to epididymal development, regionalization and maintenance of function, as revealed by GO analysis that their target genes enriched in functions of anti-apoptosis, cell transportation and development. [score:7]
Among epididymal differentially expressed miRNAs, the whole miR-200 family was more expressed in the caput, compared with cauda, which inferred a role of this miRNA family in the maintenance of epididymal regional gene expression between the two physiologically distinct regions. [score:6]
We then studied and confirmed the negative expression correlation and bona fide regulation of miR-200 family on their target genes between caput and cauda. [score:6]
Comparatively, the miR-29 family showed consistent regional expression [25] while the miR-200 family were differentially expressed. [score:5]
All the 4 genes were more expressed in the cauda than caput (Fig 6B) based on the epididymal mRNA microarray data [31], and their 3’ UTR regions contained potential target sites of the miR-200 family, in whole or in part (Fig 6C). [score:5]
This result indicated that the putative miR-200 family target genes were significantly located in the bottom of the gene list and their expression in the cauda was statistically higher than in the caput. [score:5]
Right panel: heat map of miR-200 target gene expression in caput and cauda region (Cap1-5 and Cau1-6 reflected the subdivision of each region in the study performed by Jelinsky et al., [31]). [score:5]
Luciferase reporter assay was performed to verify the bona fide regulation of miR-200 family on 4 putative target genes (Bcap29, Rab21, Slc23a1 and Dek) whose 3’ UTR regions contained potential target sites of the 5 miRNAs, in whole or in part. [score:5]
Additionally, specific miRNAs such as miR-200a [26], miR-200c [27], miR-335 [28] and miR-29a [25] were identified to regulate epididymal development by targeting β-catenin, E-cadherin, Zeb1, Nasp and etc. [score:5]
Taken together, cauda expression of the miR-200 family were 30%- 70% lower than the caput level (Fig 4B), implicating potential roles of this miRNA family in maintaining region-specific gene expression between the two regions. [score:5]
Dual luciferase reporter assay was performed to confirm the targeting and regulation of miR-200 family on 4 predicted target genes: Bcap29, Rab21, Slc23a1 and Dek. [score:5]
Left panel: enrichment score of putative miR-200 target genes against their expression profile of caput and cauda epididymis. [score:5]
GSEA analysis revealed negative expression correlation between miR-200 family and their target genes. [score:5]
Bona fide regulation of miR-200 family on 4 putative target genesThe miR-200 family comprises of 5 miRNAs: miR-200a, miR-200b, miR-200c, miR-141 and miR-429. [score:4]
This result confirmed the bona fide interaction and regulation of miR-200 family to their targets. [score:4]
Interestingly, in these studies, the miR-200 family members tended to simultaneously up- or down-regulated in response to a certain change of physiological state [39, 46]. [score:4]
Functions of miR-200 family target genes were mainly enriched in the categories of “anti-apoptosis”(8.04%, P = 0.0002) (Ets1, Stat5a, Bnip3l, Tgfa, Nr3c1, Fn1, Cited2), “carboxylic acid transport”(6.90%, P = 0.0019) (Slc23a1, Slc38a2, Slc23a2, Serinc1, Slc6a15, Slco1a5), “transmembrane receptor protein tyrosine kinase signaling pathway”(6.90%, P = 0.0063) (Txnip, Flt1, Ndst1, Efna1, Stat5a, Tgfa) and “blood vessel development”(6.90%, P = 0.0126) (Flt1, Efna1, Tgfa, Ppap2b, Cxcl12, Cited2), suggesting that miR-200 family contributed to these functional diversities between caput and cauda epididymis. [score:4]
Bona fide regulation of miR-200 family on 4 putative target genes. [score:4]
In conclusion, our study revealed a role of region-specific epididymal miRNAs, especially the miR-200 family in regulating epididymal regional gene expression in adult rats, which might contribute to the distinct physiological function in sperm maturation / storage of caput / cauda epididymis. [score:4]
As two members of the miR-200 family (miR-200a and 141) were observed, we further examined the expression pattern of the remaining three miRNAs (miR-200b, 200c and 429). [score:3]
Among them, 5 miR-200 family miRNAs, together with miR-664 and miR-327, were shown by microarray to be differentially expressed between caput and cauda epididymis. [score:3]
We performed GO enrichment analysis to further explore the potential functions of miR-200 family target genes. [score:3]
miR-200 family was more expressed in the caput than in the cauda epididymis. [score:3]
GO enrichment of miR-200 family target genes. [score:3]
Functional enrichment of miR-200 family target genes. [score:3]
Previous studies reported the epididymal temporal expression of miR-29and miR-200 families [25– 27]. [score:3]
As an important miRNA family, miR-200 miRNAs were proved to have marked biological significance in many aspects, especially in the inhibition of epithelial-mesenchymal transition (EMT) and repression of metastasis and progression of different cancer types such as ovarian and mammary cancer [39, 43– 46]. [score:3]
Results of GSEA analysis for target genes of miR-200 family. [score:3]
Result of GSEA analysis for miRNA-200 family target genes. [score:3]
7 miRNAs that met the criteria ofLog2 fold change>1 and P value<0.05 were represented in blue dots and shown in Table 3. Among them, miR-664, miR-141, miR-145, miR-148b_MM2, miR-200a showed higher expression in the caput while miR-327 and let-7c in the cauda. [score:3]
0124450.g005 Fig 5 of for target genes of miR-200 family. [score:3]
Similarly, in our study, all 5 miR-200 family miRNAs showed higher expression in the caput (Fig 4B). [score:3]
As shown in Fig 5 and Table 4, for the miR-200 targets, their enrichment score achieved -2.01 with a significant P value (0.002) and FDR (0.9%, much less than 20%) when the parameter of “metric of ranking genes” was “diff_of_Classes” and the parameter of “Enrichment statistic” was “classic”. [score:3]
In this study, we verified Slc23a1, Rab21, Bcap29 and Dek as the bona fide targets of the miR-200 family. [score:3]
In detail, Bcap29 was predicted to be targeted by miR-200a and 141, Rab21 and Slc23a1 by miR-200b, 200c and 429, and Dek by all the 5 miRNAs. [score:3]
More detailed and specific actions of miR-200 family on epididymal development, sperm maturation and storage are needed to be explored in depth in the future studies. [score:2]
0124450.g004 Fig 4 (A) The expression of miR-200a, miR-200b, miR-200c, miR-141, miR-429, miR-664, miR-327 and let-7a was examined from the IS, Cap, Cor and Cau epididymis of 5 SD rats by qPCR and compared with microarray results. [score:2]
More specifically, channel proteins such as Slc23a1, Slc38a2, Slc23a2, Slc6a15 and Slco1a5 are under the regulation of miR-200 family. [score:2]
The miR-200 family comprises of 5 miRNAs: miR-200a, miR-200b, miR-200c, miR-141 and miR-429. [score:1]
Moreover, as a powerful inhibitor of EMT and cancer metastasis and progression, whether the epididymal miR-200 family contributes to the rarity of epididymal cancer is an intriguing question that requires further investigation. [score:1]
Then the set of putative miR-200 target genes was investigated whether they were significantly sat in the top or bottom of the ranked list. [score:1]
Cells were transiently transfected with 100 ng of each of the above 4 constructs and together with respectively 40 pmol mimics of miR-200a, miR-200b, miR-200c, miR-141, miR-429 and miR-NC (Negative control miRNA, 5’- UUCUCCGAACGUGUCACGUTT -3’). [score:1]
Based on these observations, the whole miR-200 family seemed to work as a group, which might achieve amplified biological effects. [score:1]
0124450.g006 Fig 6 (A) Two subfamilies of the miR-200 family with slightly different seed regions. [score:1]
[1 to 20 of 47 sentences]
[+] score: 106
To test whether gain in regulatory microRNAs in undifferentiated BeWo cells, where the expression of the microRNAs is relatively low, lead to change in TTR expression, mature miR-200a-3p or miR-141-3p mimics were transfected into BeWo cells in the absence or presence of the respective inhibitors. [score:8]
In summary, we identified TTR as a direct target of miR-141-3p or miR-200a-3p and demonstrated that TTR and these microRNAs are reciprocally expressed during human trophoblast differentiation. [score:6]
Figure 4Overexpression and inhibition of miR-200a-3p and miR-141-3p regulate TTR and its function in human trophoblast cells. [score:6]
Successful reversal of this suppression phenomenon was observed with the addition of inhibitors for miR-200a-3p and miR-141-3p along with the respective mimics (Fig.   2b and d). [score:5]
Our data revealed that overexpression of miR-200a-3p or miR-141-3p repressed the expression of TTR in human trophoblast cells. [score:5]
Significant up-regulation of both miR-141-3p and miR-200a-3p levels was observed along with TTR down regulation in differentiating human trophoblast cells. [score:5]
Over expression of either miR-200a-3p or miR-141-3p using mimics in undifferentiated BeWo cells led to reduced expression of TTR transcript. [score:5]
These data strongly suggest that miR-200a-3p and miR-141-3p may regulate the expression of TTR and consequently TTR -mediated delivery of thyroxin hormone in placental trophoblast cells. [score:4]
Our finding that miR-141-3p and miR-200a-3p are involved in the regulation of TTR during trophoblast differentiation provides yet another mechanism by which microRNA adds a complementary layer of control at the post-transcriptional level to developmentally indispensible genes known to be transcriptionally regulated. [score:4]
Similarly microRNA inhibitors for miR-141-3p or miR-200a-3p (Ambion, USA) were transfected at a final concentration of 200 nM to prove the specificity of the microRNA action. [score:3]
To validate whether TTR mRNA is a direct target of miR-200a-3p and miR-141-3p, dual luciferase reporter assay was performed in HEK293 cells. [score:3]
These data indicate that miR141-3p and miR-200a-3p might play important roles in regulating TTR during normal placental development. [score:3]
Saha S Choudhury J Ain R MicroRNA-141-3p and miR-200a-3p regulate insulin-like growth factor 2 during mouse placental developmentMol. [score:3]
Recent studies reported that miR-141-3p, belonging to the miR-200 cluster, is overexpressed in IUGR as well as in preeclamptic placentas 42– 44. [score:3]
Our study on conserved microRNAs as plausible regulators of TTR biogenesis led to identification of two microRNAs, miR-200a-3p and miR-141-3p that directly bind to the 3′-UTR of TTR. [score:3]
In brief, BeWo cells were transfected with miR-141-3p or miR-200a-3p mimic alone or mimic plus inhibitors as described above. [score:3]
The putative binding sites for miR-141-3p and miR-200a-3p on 3′-UTRs of human and rat TTR were identified using the TargetScan mouse 6.0, PicTar, microRNA. [score:3]
Figure 3Differentiation of human trophoblast cells (BeWo) is associated with reciprocal expression of hTTR and miR-200a-3p, miR-141-3p. [score:3]
In line with our previous results, down regulation of TTR mRNA and protein upon differentiation was associated with significant up regulation of both miR200a-3p and miR-141-3p (Fig.   3f). [score:3]
Since TTR biogenesis by placental trophoblast cells is crucial for proper fetal development, our results on miR-141-3p and miR-200a-3p in regulating T [4] uptake by human trophoblast cells led to next set of experiments using IUGR rat mo del as well as in human IUGR placentas. [score:3]
This mutagenic reaction introduced two point mutations in the binding site of 141-3p and miR-200a-3p (5′-CGGTGCT-3′). [score:2]
Overexpression of either miR200a-3p or 141-3p led to almost 80% decrease in T [4] uptake by BeWo cells as early as 2 h, which persisted through 4 h time point as compared to scramble transfected cells (Fig.   4c). [score:2]
Figure 5Induction of IUGR during pregnancy in rats impacts TTR and the regulatory microRNAs, miR-200a-3p and miR-141-3p. [score:2]
Interestingly, our data highlight that in human IUGR placenta the regulation of TTR by miR-141-3p and not miR-200a-3p is physiologically relevant like that in rat. [score:2]
Mutated version of hTTR 3′UTR (5′-CGGTGCT-3′) were generated by introducing two point mutations in the seed region (5′-CAGTGTT-3′) of miR-141-3p and miR-200a-3p. [score:2]
This data clearly indicates that both miR-200a-3p and miR-141-3p have the ability to regulate endogenous TTR protein levels in human trophoblast cells. [score:2]
Cells were transfected with microRNA mimics for miR-141-3p or miR-200a-3p (Ambion, USA) individually at a final concentration of 200 nM (titrated for maximum down regulation of TTR prior to this experiment, data not shown) using Lipofectamine RNAiMAX (Invitrogen, USA) as per manufacturer’s instructions. [score:2]
MiR-141-3p or miR-200a-3p can regulate endogenous TTR protein levels as well as thyroxin uptake by human trophoblast cells. [score:2]
Both miR-141-3p and miR-200a-3p share a common microRNA response element (MRE) on the 3′UTR of TTR transcript, which is highly conserved across species including humans (Fig.   1c). [score:1]
Output from various microRNA prediction tools has been revealed that two members of miR-200 family, miR-200a-3p and miR-141-3p have conserved binding sites on the 3′UTR of TTR mRNA. [score:1]
In the first construct 14–263 nucleotide of 3′UTR of TTR containing the putative MRE for miR-200a-3p and miR-141-3p (5′-CAGTGTT-3′) was cloned downstream of the firefly luciferease reporter in the pmirGLO plasmid and was denoted as ‘wild type’. [score:1]
Leading on from this, we tested the role of miR-141-3p and miR-200a-3p in term placenta from human control and IUGR pregnancies. [score:1]
Figure 1Cellular source of TTR in developing rat placenta and miR-200a-3p, miR-141-3p binding sites on 3′-UTR of TTR mRNA (a) Quantitative real time PCR analysis of TTR mRNA from rat placental samples at different days of gestation. [score:1]
On the contrary, miR-200a-3p did not show any significant change between control and IUGR placentae (Fig.   5f). [score:1]
In contrast, miR-200a-3p remained unchanged in labyrinth zone of the placenta in control and IUGR rats indicating that miR-200a-3p is not physiologically relevant during IUGR in rat. [score:1]
These trophoblast cells can be used as an ex vivo mo del system for studying the effects of miR-141-3p and miR-200a-3p on endogenous TTR during trophoblast differentiation. [score:1]
Using various bioinformatic software, binding sites of two microRNAs, miR-141-3p and miR-200a-3p were identified to be present in the 3′-UTR of human TTR and were found to be conserved across species. [score:1]
[1 to 20 of 37 sentences]
[+] score: 99
MicroRNA-200a inhibition was performed using 5nM miR-200a -targeting and non -targeting control power inhibitors (Exiqon), transfected in tandem with a synthetic miR-200a target RenSP luciferase reporter plasmid (Switchgear Genomics, Carlsbad, CA) at a ratio of 1:5 (ng:nL) with Dharmafect Duo transfection reagent (GE Healthcare, Pittsburgh, PA). [score:11]
While expression of this miRNA increased with advancing cancer progression in rats on the ad libitum Control diet, miR-200a expression was significantly downregulated in CR tumors compared to Control tumors, indicating that the CR diet maintains miR-200a expression at levels closer to those seen in normal tissue. [score:9]
These findings deepen our understanding of the dysregulation of miRNA throughout cancer progression and suggest that miR-200a may be a novel intervention target for mimicking the suppressive effects of CR on mammary tumor development and growth. [score:7]
The majority of these progression -associated miRNAs, including miR-10a, miR10b, miR-124, miR-125b, miR-126, miR-145, were increasingly downregulated with increasing lesion severity, while 2 miRNAs, miR-21 and miR-200a, were upregulated with advancing tumor progression. [score:7]
Although the miR-200 family of miRNAs are most traditionally thought of as tumor-suppressive miRNAs because of their ability to target epithelial-to-mesenchymal transition-promoting transcripts, it is clear that miRNAs have many different functions through the targeting of hundreds of mRNAs, and thus different functions can be dominant in different biological settings [11, 28, 29]. [score:7]
When miR-200a function was inhibited in vitro in both rat and human luminal mammary cancer cell lines to mimic the effect of CR on this miRNA, cellular proliferation was significantly decreased compared to a non -targeting inhibitor control (LA7: P = 0.012, MCF7: P = 0.037)(Fig 4B and 4C). [score:6]
MiR-200a is upregulated in many types of cancerous tissue including mammary cancer, and this upregulation can contribute to tumorigenesis by affecting proliferation, oxidative stress responses, and/or resistance to cell death [30, 31, 32, 33]. [score:6]
The downregulation of progression -associated miR-200a by CR inhibits cellular proliferation. [score:6]
Further, we have shown that CR greatly reduces tumor initiation and growth, a protective effect that can be explained, at least in part, through CR’s normalization of miR-200a expression and resultant inhibition of cellular proliferation. [score:5]
This finding suggests that CR may reduce tumor burden by dampening cellular proliferation through the prevention of miR-200a upregulation. [score:4]
Moreover, we found that CR strongly suppresses DMBA -induced mammary tumor development, and that one of these progression -associated miRNAs, miR-200a, is highly responsive to CR and may be an important contributor to the anticancer effects of CR. [score:4]
However, the expression of miR-21 and miR-200a increased throughout progression, a pattern that suggests these miRNAs function as oncomiRs in this mo del. [score:3]
Specifically, miR-200a was downregulated by 57% in CR tumors compared to Control tumors (P = 0.002). [score:3]
This result indicates that miR-200a has a pro-proliferative function in mammary cancer cells and corresponds with the finding that its expression increases in vivo throughout progression of luminal mammary cancer. [score:3]
When miR-200a was inhibited in both rat and human luminal mammary cancer cell lines, mimicking CR’s effect on this miRNA, we found proliferation was significantly reduced. [score:3]
The 8 miRNAs we found from our profiling (specifically, miR-10a, miR-10b, miR-21, miR-124, miR-125b, miR-126, miR-145, and miR-200a) each showed progressive changes in expression with advancing lesion grade. [score:3]
0159686.g004 Fig 4(A), Real-time PCR quantification of tumoral miR-200a expression. [score:3]
Presently, we have shown that the regulation of miR-200a may be one such mechanism. [score:2]
In summary, we have presented, for the first time, a luminal mammary cancer progression -associated miRNA profile and have shown that CR prevents the dysregulation of one of these miRNA, miR-200a. [score:2]
Of the eight progression -associated miRNAs we identified, miR-200a was the only one found to be CR-responsive. [score:1]
Considering our results to this point, we hypothesized that miR-200a was acting as an oncomiR in this mo del and that CR’s normalization of miR-200a could be contributing to the protective effect of this dietary regimen. [score:1]
We identified 8 miRNAs that are associated with mammary tumor progression, and found that one of these, miR-200a, is associated with the potent anticancer effects of a 30% CR diet regimen. [score:1]
MiR-200a inhibition and proliferation assays. [score:1]
The 8 miRNAs we identified to be progression -associated were assessed in tumor RNA samples from Control and CR mice, and only one, miR-200a, was found to be CR-responsive (Fig 4A). [score:1]
[1 to 20 of 24 sentences]
[+] score: 84
Other miRNAs from this paper: rno-mir-26b, rno-mir-200c, rno-mir-200b
The present data showed that HQH could restore the downregulated expression of miR-200a in UUO rats and reduced ZEBs expression at 3 h and inhibited EMT at 24 h in NRK-52E cells. [score:10]
Different dosages of HQH upregulated miRNA-200a expression after obstruction (Figure 3(a)). [score:6]
HQH Upregulated miRNA-200a Expression in UUO Rats and NRK-52E Cells. [score:6]
In summary, our data demonstrate that HQH can effectively inhibit renal fibrosis in UUO rats and EMT of renal tubular cells probably by regulating miR-200a/ZEBs expression. [score:6]
The results indicate that HQH inhibited renal fibrosis and EMT probably by regulating miR-200a/ZEBs expression. [score:6]
The miR-200a expression was significantly downregulated by three quarters in obstructed kidney in UUO rats compared to sham operation rats on day 14. [score:5]
Members of miR-200 family are responsible for suppressing the translation of two members of zinc-finger E-box binding homeobox family, ZEB1/ δEF1 and ZEB2/SIP1. [score:5]
Recent studies have linked up miR-200 members to ZEBs [31] and revealed that miR-200 family mainly regulates EMT through directly targeting ZEB1 and ZEB2 mRNA. [score:5]
The miR-200a was downregulated at 3 h in NRK-52E cells stimulated with TGF- β1. [score:4]
The potential mechanism of its antifibrotic effect is involved in EMT inhibition by regulating miR-200a/ZEBs signaling in renal tubular epithelial cells. [score:4]
It is supposed that all members of miR-200 family are able to directly target ZEB1 and ZEB2 [11, 12]. [score:4]
We further showed that these therapeutic effects of HQH were probably accomplished by regulating miR-200a and ZEBs expression in cultured NRK-52E cells and UUO rat mo del. [score:4]
Downregulation of miR-200 family was found significantly on day 7 after obstruction and more obviously on day 14 in UUO rats, which is accountable for initiation of EMT in tubular epithelial cells during renal fibrosis [12, 32]. [score:4]
Recent studies indicate that all members of miR-200 family, especially miR-200a, are implicated in inhibition of mesenchymal transition in tubular epithelial cells, partially mediating through E-cadherin restoration at initiation of EMT [12]. [score:3]
The miR-200 family plays a vital role in inhibiting EMT induced by TGF- β1 in renal tubular epithelial cells. [score:3]
The miR-200a expression was examined in obstructed kidneys of UUO rats in each group by quantitative real-time PCR. [score:3]
HQH at concentration of 60, 120, and 180 ug/mL restored miR-200a expression in TGF- β1-stimulated NRK-52E cells (Figure 3(b)). [score:3]
PCR amplifications were performed under the following reaction conditions: 95°C for 2 min; 40 cycles at 95°C for 15 s, 60°C for 30 s, and 72°C for 30 s. The miRNA-200a was quantitatively detected with All-in-One miRNA qPCR detection Kit according to the manual. [score:1]
It indicated that HQH sustained miRNA-200a levels during EMT in renal fibrosis. [score:1]
Emerging evidences revealed that miR-200 plays a vital role in maintaining epithelial phenotype. [score:1]
[1 to 20 of 20 sentences]
[+] score: 59
Cluster analysis of over-expressed miRNAs (Figure S1A) and under-expressed miRNAs (Figure S1B) indicated that some deregulated miRNAs might play their roles in groups, such as up-regulated miR-10b and miR-21 and down-regulated miR-200a* and miR-148b*. [score:12]
The proven targets of seven validated, deregulated miRNAs are listed in Table 4. Among these targets, we detected the targets of miR-200a* (the most down-regulated miRNA) in both SP cells. [score:11]
In contrast to the miR-200a* expression, both targets ZEB1 and ZEB2 were expressed at much higher levels in SP-HCCs than in SP-NLCs by sQRT-PCR (Figure S2). [score:7]
In this study, the targets of miR-200a*, ZEB1 and ZEB2 were both expressed at much higher levels in SP-HCCs than in SP-NLCs. [score:5]
The ZEB-miR-200 feedback loop has been demonstrated to link EMT activation and the maintenance of stemness by suppressing stemness-inhibiting miRNAs and acting as a promoter of mobile, migrating CSCs [59]. [score:5]
Among these targets, the miR-200a* target genes ZEB1 and ZEB2 [32], [33] were analyzed in both SP-HCCs and SP-NLCs by sQRT-PCR. [score:5]
Two important miRNAs that were down-regulated in SP-HCCs, miR-200a* and miR-148b*, have been described in HCC tissues [26] and ovarian cancers [47]. [score:4]
These data indicate that the greatly down-regulated miR-200a* may promote malignant transformation of SP-NLCs and force SP-HCCs to become more metastatic. [score:4]
Figure S2 The target analysis of miR-200a*. [score:3]
Mol Biol Cell 33 Bendoraite A Knouf EC Garg KS Parkin RK Kroh EM 2010 Regulation of miR-200 family microRNAs and ZEB transcription factors in ovarian cancer: evidence supporting a mesothelial-to-epithelial transition. [score:2]
Recent findings have associated miR-200a* with stem cell maintenance and suggest a connection between the epithelial-to-mesenchymal transition (EMT) and stem cell formation. [score:1]
[1 to 20 of 11 sentences]
[+] score: 58
It has been suggested that different cell lines regulate miR-200 expression through distinct epigenetic mechanisms [27]. [score:4]
Downregulation of miR-200 family members might underlie kidney cyst formation in Dicer mutant kidneys. [score:4]
Members of the miR-200 family were highly expressed in the kidney, lung, small intestine, and exocrine glands (Figure 2(a)). [score:3]
Members of the miR-200 family are commonly expressed in tubular tissues, and it is impossible to classify these tissues using only the miR-200 family. [score:3]
The miR-200 family consists of five members (miR-200a, miR-200b, miR-200c, miR-141, and miR-429), which are clustered and expressed as the miR-200b-200a-429 cluster at chromosomal location 1p36 and the miR-200c-141 cluster at chromosomal location 12p13. [score:3]
In human tissues, the results of the miRNA array analysis showed that miR-200a, miR-200b, and miR-200c (miR-200 family) were highly expressed in the kidney, lung, salivary gland, trachea, colon, prostate, liver, and pancreas (Figure 1). [score:3]
As expected, members of the miR-200 family were highly expressed in exocrine glands and epithelial cells. [score:3]
The expression of miR-200a, miR-200b, miR-200c, miR-192, miR-194, and miR-449a was validated with real-time RT-PCR in rat tissues in order to discriminate the kidney from other tissues with a tubular structure. [score:3]
Members of the miR-200 family were highly expressed in the proximal tubule. [score:3]
Members of the miR-200 family were expressed at high levels in each tissue with a tubular structure (Figures 3(a)– 3(c)). [score:3]
To examine the miR-200 family in the kidney, miRNA array analysis was performed to compare expression in the proximal tubule and mesangial cells. [score:3]
The lacrimal gland and salivary gland are formed from the ectoderm, and the expression ratio of miR-200a/b and miR-200c might depend on the germ layer. [score:3]
Our results showed that miR-200 family members were expressed at high levels in various tissues with a tubular structure: the kidney (proximal tubule and collecting duct), lung, pancreas (duct cells), small intestine (intestinal villus), bile duct, and exocrine glands (duct cells). [score:3]
Members of the miR-200 family are highly expressed in the kidney and lung. [score:3]
On the other hand, urinary miR-200a increased after day 3 of administration (Figure 5(c)). [score:1]
Furthermore, the levels of miR-200a/b/c were higher in the proximal tubule than in the glomerulus. [score:1]
In our results, urinary miR-200a also increased, and the sensitivity was similar to that of urinary albumin excretion. [score:1]
We assessed whether the plasma concentrations of miR-200a, miR-200b, and miR-200c could be used as a biomarker for acute kidney injury (Figure 4). [score:1]
Plasma miR-200a was not detected (data not shown). [score:1]
We assessed whether the urinary concentrations of miR-200a and miR-200c could be used as a biomarker for renal tubular dysfunction (Figure 5). [score:1]
A significant increase in plasma miR-200a/b/c, miR-192, and miR-194 levels was observed in the AKI mo del. [score:1]
These results suggest that the miR-200 family is closely associated with tubular structure. [score:1]
The concentrations of miR-200a/b/c were estimated based on the analytical curve for synthetic miRNA. [score:1]
Although morphological changes were not observed and miR-200a was not detected in plasma, macrophage infiltration was induced [23]. [score:1]
In the future, we will assess the potential of the urinary miR-200 family as biomarkers of the renal tubular dysfunction in humans. [score:1]
Patel et al. have reported that miR-200 family members play important roles in renal tubule maturation by repressing Pkd1 in the kidney [25]. [score:1]
We assessed whether the miR-200 family could be used as a biomarker for kidney injury. [score:1]
Consistently, the plasma concentrations of the miR-200 family members and miR-192 and miR-194 increased significantly. [score:1]
[1 to 20 of 28 sentences]
[+] score: 57
Other miRNAs from this paper: rno-mir-141, rno-mir-192, rno-mir-200c, rno-mir-200b, rno-mir-429
Thus, in the glomeruli, in parallel to the enhanced expression of TGF-β1, a known inducer of EMT in epithelial cells [35], [36], we found downregulation of miR-200 family members and upregulation of ZEB2 that are, respectively, essential to maintain the normal epithelial phenotype and the EMT-inducing transcriptional factor [18], [20], [36], [37]. [score:9]
The downregulation of the microRNA-200 family, in response to enhanced TGFβ 1 expression, results in the reduction of epithelial markers and enhancement in mesenchymal markers and in ZEB 2, an EMT mediator. [score:6]
The fetal-programmed adult rats showed pronounced structural glomerular disorders with an accentuated and advanced stage of fibrosis, which led us to state that the glomerular miR-200 family would be downregulated by TGF-β1 action inducing ZEB 2 expression that may subsequently cause glomerular EMT. [score:6]
Additionally, in the present study, we demonstrated a significant enhancement in the expression of mesenchymal protein markers, including fibronectin, collagen 1 [α]1 and collagen 1 [α]2. Corroborating the present findings, Xiong et al. (2012) also verified downregulation of the miR-200 family induced by TGF-β1 in kidney cell culture [38]. [score:6]
The current study has shown that LP rats present a significant downregulation of miR-141 (71%), miR-200a (50%), miR-200b (60%) and miR-429 (59%). [score:4]
Members of the miR-200 family and miR-192 act as protectors of the normal epithelial phenotype and are markedly downregulated in TGF-β -induced EMT [16], [17]– [21]. [score:4]
Expression Profile of the miR-200 Family and of miR-192 in Isolated Glomeruli. [score:3]
In isolated glomeruli, of 16-wk-old LP animals, miR-141, miR-200a, miR-200b and miR-429 were significantly down-regulated compared to NP offspring (Figure 9). [score:3]
Expression levels of mir-192, mir-141, mir-200a, mir-200b, mir-200c and mir-429 estimated by TaqMan RT-qPCR in isolated glomeruli of 16-wk old LP rats. [score:3]
0071310.g009 Figure 9 Expression levels of mir-192, mir-141, mir-200a, mir-200b, mir-200c and mir-429 estimated by TaqMan RT-qPCR in isolated glomeruli of 16-wk old LP rats. [score:3]
Expression of the miR-200 family and miR-192. [score:3]
The miR-200 family members target both ZEB1 and ZEB2 (39). [score:3]
As miRNAs have been suggested as playing a key role in a variety of kidney diseases, we investigated the expression of the miR-200 family and miR-192 in isolated glomeruli from LP compared to NP offspring. [score:2]
Each cDNA of miRNA-200 family (miR-200a, miR-200b, miR-200c, miR-141 and miR-429) and miR-192 was quantified by real-time quantitative PCR using ABI Prism 7900 Sequence Detection System (Life Technologies, USA). [score:1]
The miR-200 family is divided into two groups according to their sequence seed: group 1 (miR-141 and miR-200a) and group 2 (miR-200b, miR-200c and miR-429) (38). [score:1]
[1 to 20 of 15 sentences]
[+] score: 56
In contrast, miR-200a-3p expression, and potentially the expression of all miRNAs specified by the three clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429, tend to be up-regulated with similar FCEs in both experimental conditions. [score:8]
On the other hand, intra-cerebroventricular (ICV) infusion of anti-miR-200a-3p to Lep° [b]/Lep° [b] mice restored the hypothalamic expression of Irs-2 and Lepr, and up-regulated the hypothalamic expression of Zfpm2, Insr, Pomc, and Npy. [score:8]
Of note, the miRNAs miR-429, −182, −183-3p, −183-5p, and −96-5p which expression co-varied with that of with miR-200a-3p in all expression profiles (see above) also displayed similar FCEs (ranging from 2.8 to 6.2) and padj-values (>1.0E-2 but <5.0E-2). [score:5]
Co-variation of miRNA expression also demonstrated that the transcription and maturation of clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429 are co-regulated in ARC. [score:4]
In contrast, miR-200a-3p and −409-5p displayed trends to expression differences (padj-values > 1.0E-2 but < 5.0E-2) between groups C-C or C-HF on one hand and groups HF-C or HF-HF on the other hand. [score:3]
Pomc and miR-200a-3p expressions did not display any correlation or anti-correlation in groups C-C, C-HF, HF-C, and HF-HF of our study (R [2] = 0.09). [score:3]
We also reported up-regulation of miR-200a-3p,−200b-3p, and−409 in the hypothalamus of Lep° [b]/Lep° [b] mice deficient in leptin production when compared to Lep° [b]/Lep [+] or Lep [+]/Lep [+] mice (Crépin et al., 2014). [score:3]
Altogether our new and previous findings point to a trend to the long-term overexpression of clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429 in the ARC of adult rats and mice having experienced low levels of leptin/leptin signaling during the perinatal period. [score:3]
The increase of Pomc expression in infused mouse hypothalami may be due to the use of over-physiological quantities of anti-miR-200a-3p. [score:3]
The over -expression of miR-200a in the hypothalamus of ob/ob mice is linked to leptin and insulin signaling impairment. [score:3]
Punctual mutation or deletion in cluster miR-96/182/183 produces ear or retina disorders while loss of function of the miR-200 family leads to defects in the terminal differentiation of olfactory precursors (Choi et al., 2008; Kuhn et al., 2011; Lumayag et al., 2013). [score:2]
Members of the miRNA-200 family regulate olfactory neurogenesis. [score:2]
In these groups, miRNAs produced from clusters miR-96/182/183, miR-141/200c, miR-200a/200b/429 also appeared as hypervariable miRNAs (see Table 2). [score:1]
Figure 5 The specific case of the miRNAs specified by clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
miRNAs specified by clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429 have been identified as miRNAs of functional importance in sensory organs. [score:1]
Among the 15 (3.6%) miRNAs displaying MAX/MINs larger than this value, 8 were produced from three miR gene clusters, namely the miR-96/182/183 cluster and the two evolutionary-related clusters miR-141/200c and miR-200a/200b/429 (Table 2). [score:1]
The specific case of clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
Along with miR-200a-3p, the miRNAs miR-200a-5p, −200b-3p, −200b-5p, and −429 that are specified by the same gene cluster displayed similar FCEs (ranging from 2.0 to 3.4) and padj-values. [score:1]
Among those miRNAs were all the 10 miRNAs produced from miR gene clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
miRNAs miR-200a-3p and miR-141-3p displayed MAX/MINs higher than the value of 8.3 in groups HF-C and/or HF-HF. [score:1]
Ten miRNAs are produced by clusters miR-96/182/183, miR-141/200c, and miR-200a/200b/429. [score:1]
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[+] score: 53
As depicted in Fig 8, miR-1, miR-29a, miR-106b and miR-200a was selectively inhibited by H [2]0 [2] treated Pitx2 -overexpressing cells but up-regulated in H [2]0 [2] treated Pitx2 silenced cells at both time points (12h and 24h). [score:8]
HL-1 atrial cardiomyocytes transfected with miR-29 and miR-200 (Fig 8) significantly down-regulate Cacna1c, Hnc4 and Ryr2 expression, while Camk2a was significantly decreased with miR-200 but not miR-29 (Fig 8). [score:6]
We provide herein evidences that miR-29 and miR-200 over -expression also contributes to ion channel expression remo deling. [score:5]
Observe that miR-29 and miR-200 over -expression leads to significant decreased of Cacna1c, Hcn4, Ryr2 and Camk2a (except for miR-29a) expression. [score:5]
miR-29 over -expression in HL1 atrial cardiomyocyte deregulate Cacna1c, Hnc4 and Ryr2, influencing therefore both the calcium handling and pacemaker activity, whereas miR-200 regulated Cacna1c, Ryr2 and Camk2a, in addition to Scn5a as previously reported [64], impacting therefore also in calcium handling. [score:5]
qPCR of left atrial chambers demonstrated that miR-1, miR-26b, miR-29a, miR-30e, miR-106b, miR-133 and miR-200 are up-regulated in HTD rats as compared to controls (Fig 1), demonstrating a similar microRNA expression profile as in atrial-specific Pitx2 deficient mice [14, 16]. [score:5]
HL-1 cells (6 × 10 [5] cells per well) were transfected with plasmids containing expression constructs for Pitx2, Wnt8a (Addgene), Wnt11a (Addgene, Cambridge, MA, USA), premiR-29a, pre-miR-200 (Exiqon) or siRNA-Pitx2c, siRNA-Zfhx3, siRNA-Enpep, siRNA-Sod2 (Sigma, Aldrich, Munich, Germany) as previously described [14, 34]. [score:3]
Thus these data demonstrate that miR-29 and miR-200 impaired expression also contributes to develop pro-arrhythmogenic substrates. [score:3]
miR-29a and miR-200 expression in HL-1 atrial cardiomyocytes transfected cells. [score:3]
Whereas it is wi dely documented that redox signaling can compromise ion channel functioning and calcium homeostasis in cardiomyocytes [67], in our system we observed no influence of H [2]O [2] administration on the regulatory impact of Pitx2 in distinct ion channels such as Scn5a, Kcnj2 and Cacna1c as well as multiple Pitx2-regulated microRNAs such as miR-1, miR-26, miR-29 and miR-200, in which redox impairment impact is less documented [68]. [score:3]
We have previously demonstrated that Pitx2 modulates expression of miR-29 and miR-200, among other microRNAs [16] and furthermore we have demonstrated in this study that modulation of distinct ion channel is greatly influenced by H [2]0 [2] administration while microRNA signature is mostly dependent on Pitx2c but not H [2]0 [2] administration. [score:3]
Several lines of evidence have already reported the key regulatory role of miR-1 [60– 62], miR-26 [63], miR-106b [64], miR-133 [65– 66] and miR-200 [64] in arrhythmogenesis. [score:2]
Modulation of miR-29 and miR-200 alters cardiac action potential determinants. [score:1]
Importantly, miR-29 and miR-200 are not significantly impaired in SHR atrial chambers, suggesting that Wnt-microRNA might be a pivotal candidate establishing fundamental differences between HTD and HTN in atrial arrhythmogenesis susceptibility. [score:1]
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[+] score: 37
miR-200 family members, including the downregulated miR-200a, are predicted to target genes that regulate synaptic function, neurodevelopment and neuronal survival [50]. [score:8]
Main miR-200 family target genes in the uterus, Stat5b, Zeb1 and Zeb2, were downregulated by multigenerational stress in the F1 generation. [score:6]
Furthermore, ZEB1 serves as transcription factor to inhibit the miR-200 family, thus enhancing Stat5b expression [19]. [score:5]
The qRT-PCR confirmed changes of the selected miRNAs (Figure  4B), decreased expression of miR-96, miR-141, miR-182, miR-183, miR-200a, miR-200b, miR-429 and miR-451 in F2-SSS compared to F0-S animals, whereas miR-23b and miR-200c showed increased expression levels. [score:4]
Including the downregulated miR-200b, the miR-200 family may exert peripheral effects to control uterine quiescence and contractility during pregnancy and labour [18]. [score:4]
Furthermore, stress altered miRNA expression patterns in the brain and uterus of F2 mothers, including the miR-200 family, which regulates pathways related to brain plasticity and parturition, respectively. [score:4]
Target genes of the miR-200 family include three particular genes, Stat5b, Zeb1 and Zeb2, all involved in pregnancy maintenance [18]. [score:3]
In order to validate miRNAs, we performed quantitative real time PCR (qRT-PCR) analysis of these differentially regulated miRNAs (n = 3 per group for F0, F1 and F2 generations, three replicates per sample): miR-23b, miR-96, miR-141, miR-181a, miR-182, miR-183, miR-200a, miR-200b, miR-200c, miR429 and miR-451. [score:2]
Ancestral programming by stress particularly involved the miR-200 family. [score:1]
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[+] score: 36
In B13 cells, the absence of the expression of all members of the miR-200 family correlated with higher expression levels of Zeb1 and Zeb2 and reduced expression of both E-cad mRNA and protein levels compared to its parental cell line. [score:6]
The analysis of differentially expressed miRNAs between AR42J and B13 cells by using revealed specific expression of all the members of the miR-200 family (miR-200a, miR-200b, miR-200c, miR-141-3p, miR-141-5p and miR-429) in the parental cell line AR42J, whereas none of these miRNAs were detected in the B13 subclone. [score:5]
These cell lines presented a minimum of 59 miRNAs differentially expressed, and the plasticity of B13 cells could be explained, at least partially, by repression of the miRNA-200 family and E-cadherin as well as increased expression levels of Zeb1/Zeb2. [score:5]
miR-200 family members target and inhibit ZEB1 and ZEB2 factors which are key factors in epithelial-to-mesenchymal transition (EMT) [33– 35]. [score:5]
Moreover, miR-200 family members target and inhibit ZEB1 and ZEB2 factors, which blocks epithelial-mesenchymal transition (EMT) and causes cells to maintain an epithelial state [33– 35]. [score:5]
The expression levels of Zeb1 and Zeb2 were significantly higher in the B13 subclone compared to AR42J cells (2.7- and 57-fold, respectively) (Fig 5A and 5B), whereas expression of E-cad was 52-fold lower (Fig 5C), which agree with the expected biological activity of miR-200 family in each cell type. [score:4]
Notably, all members of the miR-200 family (miR-200a, miR-200b, miR-200c, miR-141-3p, miR-141-5p and miR-429), which has been shown to be enriched in differentiated tissues such as ectoderm and endoderm and is largely excluded from the mesoderm [30– 32], were specifically expressed in AR42J cells and absent in the B13 subclone. [score:3]
There is strong evidence demonstrating that expression of the miR-200 family is enriched in terminally differentiated cells, such as epithelial tissues, and that it is undetected in pluripotent cells, such as mesenchymal cells [30– 32]. [score:3]
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[+] score: 32
mir-200a, mir-34, mir-195, and mir-381-3p are usually downregulated in presence of SIRT1 expression, and vice versa low expression of SIRT1 relates to miRNAs upregulation [9, 11, 17, 18, 26– 28]. [score:11]
Comparing the miRNAs expression of LPS -treated rats with LPS + RvD1, a significant downregulation of the levels of miR-195-5p, miR-200a-3p (related to SIRT1 expression and activity), miR-145-5p (related to both SIRT1 and p53 regulation), and miR-34a-5p (candidate for p53 regulation) in ocular tissues of LPS + RvD1 1000 ng/kg treated rats compared to the LPS -treated group (P < 0.01 versus LPS group; Figure 6) was noted. [score:9]
Interestingly, the protective action of intravitreal RvD1 was associated with an increased level of endogenous SIRT1 within the eye and a downregulated expression of miR-195-5p, miR-200a-3p, miR-34a-5p, and miR-145-5p. [score:6]
These miRNAs are notoriously and inversely related to SIRT1 expression in tissues as, for example, 195-5p and miR-200a-3p relate to SIRT1 expression and activity, miR-145-5p relates to SIRT1 and p53 levels, and miR-34a-5p relates to p53 regulation [9– 11]. [score:6]
[1 to 20 of 4 sentences]
[+] score: 31
Collectively, chronic alcohol consumption superimposed on overnutrition -mediated cardiac pathology can putatively induce the following signaling mechanisms: (1) inhibition of mTORC1 and attenuation of protective compensatory mechanisms; (2) inhibition of INS metabolic signaling via downregulation of INS receptor, IRS-1, GLUT4; (3) downregulation of growth inhibitory mir-200 family microRNAs and (4) upregulation of mir-212 (Figure 4). [score:16]
The mir-200c also regulates stem cell factors, and it has been proposed that targeting the ZEB1-miR-200 feedback loop can lead to a promising treatment for fatal tumors, such as pancreatic cancer [98]. [score:4]
Another effect of alcohol is its ability to downregulate mir-200a [113, 114] as shown by studies involving Lieber-DeCarli diet -induced alcoholic steatohepatitis mice mo dels. [score:4]
Therefore, downregulation of mir-200 family microRNAs by alcohol can potentially increase growth and S6K1 protein levels. [score:4]
The mir-200 family microRNAs are shown to function as inhibitors of growth in many cell types. [score:3]
[1 to 20 of 5 sentences]
[+] score: 26
In detail, five miRNAs were significantly up-regulated (miR-21, miR-34c-3p, miR-470*, miR-10b, let-7i*) and two miRNAs significantly down-regulated in SP of HCC cells (miR-200a*, miR-148b*). [score:7]
Previous studies have linked the miR-200 family with the epithelial phenotype [34], and Korpal et al. [35] identified miR-200a as a suppressor of epithelial-mesenchymal transition (EMT) through direct targeting of ZEB1 and ZEB2 genes. [score:6]
of the down-regulated miR-200a*, and miR-148b* in SP of HCC cells had the fold changes 0.1 ± 0.04, and 0.4 ± 0.08, respectively (P < 0.01). [score:4]
A subset of miRNAs was also identified and shown to be significantly underexpressed in our study, including miR-200a and miR-148b*. [score:3]
These target genes were PTEN (miR-21), P53 (miR-34c), Rho C (miR-10b), RAS (let-7i), and ZEB1 (miR-200a). [score:3]
Ten miRNAs were underexpressed, including miR-200a* and miR-148b*. [score:3]
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[+] score: 24
In epithelial cells, miR-200 family microRNAs and E-cadherin maintain higher level expression by repressing ZEB1, ZEB2 and TGFβ; on the other hand, in mesenchymal cells and tumors, the up-regulation of ZEB factors is triggered by TGFβ and suppresses the transcription of miR-141/200c by binding to their putative common promoter region. [score:8]
In our primary dataset, ZEB1 and ZEB2 were both up-regulated in six out of our eight ccRCC samples and, their expression levels were highly anti-correlated with the miR-200 family in both tumor and normal samples. [score:6]
Recently, several other groups have reported a role for the miR-200 family in the Epithelial-Mesenchymal-transition (EMT) and in cancer cell migration, the latter by directly targeting the transcription factors ZEB1 and ZEB2, which regulate E-Cadherin, a mediator of cell-cell adhesion [84, 85]. [score:5]
We also noted that in our data, the anti-correlation between VEGFA and the miR-200 family was strongest in normal kidney tissue, suggesting that loss of this regulation may be an important factor providing a permissive environment for HIF transcriptional signaling. [score:2]
We also found strong anti-correlation between VEGFA and the miR-200 family of microRNA: miR-200a*, 200b, 200c and miR-141. [score:1]
Five miR-200 family members contain very similar seed sequences - AAUACU for miR-200b/200c/429 and AACACU for miR-200a*/141 [84]. [score:1]
Another example is the miR-200 family which includes two microRNA clusters, one on Chromosome 1p36.3 (miR-200a*/200b/429) and another on Chromosome 12p13 (miR-200c/141). [score:1]
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[+] score: 21
miR-429 was indicated to regulate 26 downregulated DEGs (P=1.52×10 [−10]), and miR-200a and miR-141 regulated 23 downregulated DEGs each, with P-values of 8.7×10 [−8] and 1.4×10 [−8], respectively. [score:9]
Benoit et al (35) have reported the upregulation of rno-miR-200a in rats on a high-fat diet. [score:4]
Thus, it is presumed that there may be a certain correlation between rno-miR-200a and the downregulation of cholesterol metabolism -associated genes over time. [score:4]
However, no targets of miR-200a, miR-429 and miR-141 were observed in the cholesterol metabolism -associated DEGs observed in the present study, which may be attributed to the small sample size of the microarray used. [score:3]
miR-429, miR-141 and miR-200a belong to the same miR-200 family. [score:1]
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[+] score: 18
Increasing expression of miR-200a and miR-30a may combine to repress expression of Sox11, thereby decreasing stimulation of Pax5. [score:5]
0125153.g009 Fig 9(A) Log2 plots of microarray and qPCR expression profiles for miRNAs and their predicted target genes: miR-214, and Xbp1; miR-29c, miR-200c and Klf4; and miR-30a, miR-200a, and Sox11. [score:5]
The network suggests a molecular switch (involving Prdm1, Sox11, Pax5, miR-200a, and miR-30a) progressively decreases repression of Xbp1 gene transcription, in concert with decreased translational repression by miR-214. [score:3]
Sox11 expression was elevated in embryonic stage acinar cells, decreasing dramatically immediately after birth apparently due to concerted action by both miR-200a and miR-30a. [score:3]
Assays with miR-200a, and miR-30a did not show any repression of the reporter, however, a construct containing binding sites for both miR-200a and miR-30a was repressed when co -transfected with both miRNAs (Fig 9B), indicating that these miRNAs are acting cooperatively to repress expression. [score:2]
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[+] score: 17
Other miRNAs from this paper: mmu-mir-200a
Figure 7 (A) Expression of vimentin and N-cadherin in K3, K3-F4, and K3-B6 cells was detected by immunofluorescence analysis (×200); (B) Expression of vimentin, N-cadherin, and E-cadherin in K3, K3-F4, K3-B6 cells was detected by; (C) Expression of miRNA-200a, snail, slug, and ZEB1 in K3, K3-F4, and K3-B6 cells was detected. [score:7]
In addition, the expression level of the accepted EMT inhibitor miR-200a was lower in K3-F4 and K3-B6. [score:5]
Moreover, the expression levels of miR-200a, an accepted EMT inhibitor, were lower in K3-F4 and K3-B6 cells than in K3 cells (Figure 7C). [score:5]
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[+] score: 15
Previous studies have shown that in fibrotic renal tissues the expressions of both miR-200 family and E-cadherin are significantly downregulated and that exogenous miR-200 could reduce renal fibrosis [30, 31]. [score:6]
Gregory PA Bert AG Paterson EL Barry SC Tsykin A Farshid G The miR-200 family and miR-205 regulate epithelial to mesenchymal transition by targeting ZEB1 and SIP1Nat Cell Biol. [score:4]
Park SM Gaur AB Lengyel E Peter ME The miR-200 family determines the epithelial phenotype of cancer cells by targeting the E-cadherin repressors ZEB1 and ZEB2Genes Dev. [score:3]
Pre-transfection of the miR-200 family can reverse TGF-β1 -mediated EMT in tubular epithelial cells [30, 32, 33]. [score:1]
Mongrco PS Rustgi AK The role of the miR-200 family in epithelial—mesenchymal transitionCancer Bid Ther. [score:1]
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[+] score: 15
Similarly, the expression of oncogenic miRNAs like miR-21, miR-10b, let-7i, miR-34c, were increased more than 2 fold in EpCAM [+] liver cancer cells; whereas miR-125b, miR-200a, miR-148b were most down-regulated. [score:6]
The miR-200a was observed regulates epithelio-mesenchymal to stem-like transition in nasopharyngeal carcinoma cells by targeting ZEB2 and ß-catenin signaling genes [30]. [score:4]
In addition, the miR-200a and miR-148b were significantly underexpressed in EpCAM [+] liver cancer cells compared to fetal liver cells (P<0.05) [22]. [score:2]
In our later study, we are planning to combine the miR-92b with miR-200a or miR-21 to search for the mechanisms of malignant transformation. [score:1]
miRNA-200a and miR-21 were found to be involved in the malignant transformation of liver stem cells. [score:1]
Our data showed that the mir-92b might contribute to the malignant transformation of the liver stem cells, which may be a new valuable marker of HCC, and the analogy between the already confirmed miRNAs such as antioncogene mir-200a [45] or Oncogene mir-21 [46]. [score:1]
[1 to 20 of 6 sentences]
[+] score: 15
Other miRNAs from this paper: rno-mir-200c, rno-mir-200b
Liu et al. [32] reported that they selected mRNAs with a conserved seed sequence in their 3′-UTRs for miRNAs that were diversely expressed between tumor and normal kidney, and identified target mRNAs whose expression had an negative correlation with that of miR; they found that there was an obvious inverse correlation between the miR-200 family and VEGF. [score:7]
Figure 2The targeting relationship between miR-200b and VEGFA geneNote: (A) The VEGFA 3′-UTR loci for combining miR-200b; (B) The luciferase expression was detected 48 h after 293T cells were co -transfected with VEGFA-3′-UTR-WT plasmid + miR-200 mimics plasmid, VEGFA-3′-UTR-MUT + miR-200b/NC; ** P<0.05 was considered statistically significant. [score:4]
The miR-200 family, including miR-200b, is a cluster of miRNAs, which are highly associated with epithelial–mesenchymal transition (EMT), wherein miR-200b was thought to be a key negative regulator of tumor metastasis, invasion, and chemo-sensitivity [7]. [score:2]
Note: (A) The VEGFA 3′-UTR loci for combining miR-200b; (B) The luciferase expression was detected 48 h after 293T cells were co -transfected with VEGFA-3′-UTR-WT plasmid + miR-200 mimics plasmid, VEGFA-3′-UTR-MUT + miR-200b/NC; ** P<0.05 was considered statistically significant. [score:2]
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[+] score: 13
Members of the miR-200 family are known to suppress the Zeb2 transcription factor, and its inhibition promotes MET [53]. [score:5]
Among the miRNAs upregulated in rat PSCs, we also identified miR-205 and members of the miR-200 family (miR-200a, miR-200b, miR-200c, miR-141 and miR-429), which promote mesenchymal to epithelial transition (MET) in mouse cells, a key step in fibroblast reprogramming [47]. [score:4]
A number of miRNAs that were found to be upregulated in rat PSCs, such as the miR-290-295 cluster and the miR-200 family miRNAs, are involved in pluripotency induction and maintenance in mice 21, 47. [score:4]
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[+] score: 13
Another highly-enriched beta cell miRNA is miR-200a, demonstrated to be upregulated in islets of the db/db diabetic mouse mo del and shown to contribute in regulating pancreatic beta cell survival in T2D (Belgardt et al., 2015). [score:5]
Expression of miR-200a, miR-130a and miR-152 in INS-1 832/13 cells (A–C) or in EndoC-βH1 cells (D–F) at different confluences. [score:3]
For miR-200a, miR-130a and miR-152, the expression levels were found not to be influenced by cellular confluence (Fig. S2). [score:3]
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]
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]
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[+] score: 12
In addition, Yuan et al. (19) determined that miR-200a could upregulate global histone H3 acetylation levels through directly targeting the 3′ untranslated region of the HDAC4 messenger RNA and repressing expression of HDAC4 in hepatocellular carcinoma. [score:11]
Excitingly, the histone H3 acetylation levels at the promoter of miR-200a itself were also increased through an Sp1 -dependent pathway that consequently activates its own transcription. [score:1]
[1 to 20 of 2 sentences]
[+] score: 11
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-17, hsa-mir-21, hsa-mir-22, hsa-mir-28, hsa-mir-29b-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-145a, mmu-mir-150, mmu-mir-10b, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-206, mmu-mir-143, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-217, hsa-mir-218-1, hsa-mir-223, hsa-mir-200b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-143, hsa-mir-145, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-150, hsa-mir-195, hsa-mir-206, mmu-mir-200a, 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-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-22, mmu-mir-29c, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-331, mmu-mir-331, rno-mir-148b, mmu-mir-148b, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-10a, mmu-mir-17, mmu-mir-28a, mmu-mir-200c, mmu-mir-218-1, mmu-mir-223, mmu-mir-199a-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, mmu-mir-217, hsa-mir-29c, hsa-mir-200a, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-135b, hsa-mir-148b, hsa-mir-331, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-10a, rno-mir-10b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-22, rno-mir-28, rno-mir-29b-1, rno-mir-29c-1, rno-mir-124-3, rno-mir-124-1, rno-mir-124-2, rno-mir-133a, rno-mir-143, rno-mir-145, rno-mir-150, rno-mir-195, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-206, rno-mir-217, rno-mir-223, dre-mir-7b, dre-mir-10a, dre-mir-10b-1, dre-mir-217, dre-mir-223, hsa-mir-429, mmu-mir-429, rno-mir-429, mmu-mir-365-2, rno-mir-365, dre-mir-429a, hsa-mir-329-1, hsa-mir-329-2, hsa-mir-451a, mmu-mir-451a, rno-mir-451, dre-mir-451, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-1-2, dre-mir-1-1, dre-mir-9-1, dre-mir-9-2, dre-mir-9-4, dre-mir-9-3, dre-mir-9-5, dre-mir-9-6, dre-mir-9-7, dre-mir-10b-2, dre-mir-16a, dre-mir-16b, dre-mir-16c, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-22a, dre-mir-22b, dre-mir-29b-1, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-133a-2, dre-mir-133a-1, dre-mir-133b, dre-mir-133c, dre-mir-143, dre-mir-145, dre-mir-150, dre-mir-200a, dre-mir-200b, dre-mir-200c, dre-mir-206-1, dre-mir-206-2, dre-mir-365-1, dre-mir-365-2, dre-mir-365-3, dre-let-7j, dre-mir-135b, rno-mir-1, rno-mir-133b, rno-mir-17-2, mmu-mir-1b, dre-mir-429b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-9b-2, rno-mir-133c, mmu-mir-28c, mmu-mir-28b, hsa-mir-451b, mmu-mir-195b, mmu-mir-133c, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-451b, mmu-let-7k, rno-let-7g, rno-mir-29c-2, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
For example, in mouse [14], miR-10b is highly expressed in spinal cord; miR-124 is wi dely expressed in brain tissues; miR-200b, miR-128a, miR-128b, miR-429 are specifically expressed in olfactory bulb; miR-200a is highly expressed in olfactory bulb; miR-7b is highly expressed in hypothalamus. [score:11]
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[+] score: 9
ZEB1 and ZEB2 mRNAs are well-described targets of the miR-200 family, and many reports have suggested that miR-200 family members block EMT by inhibiting ZEB1 and ZEB2 expression [15]. [score:7]
Of note, the miR200/MALAT1 sponge mediating the EMT processes in endometriosis is complex and never exclusive. [score:1]
Notably, endometrial stromal β-catenin is required for steroid -dependent mesenchymal–epithelial crosstalk and decidualization [33]; whether the LPAR3/β-catenin pathway also contributes to the EMT processes in endometriosis and its possible crosstalk with the miR200/MALAT1 sponge requires further research. [score:1]
[1 to 20 of 3 sentences]
[+] score: 8
MiR-200a targets ZEB2, and miR-21 targets BCL2. [score:5]
al, 3 miRNAs were differentially expressed in human esophageal adenocarcinoma: miR-200a, miR-21, and miR-133a. [score:3]
[1 to 20 of 2 sentences]
[+] score: 8
Indeed, an analysis of TargetScan revealed that the lesion in l11Jus05 lies within a seed sequence for the microRNA miR200 [13], [14]. [score:3]
Further studies of this mutation will help us to determine how miR200 regulates Med13. [score:3]
MiR200 is required for the mesenchymal/epithelial transition during embryonic development and is involved in cancer metastasis [38], [39]. [score:1]
We report the first lesion in a miR200 seed sequence in the 3′ UTR of Med13 in the lethal line l11Jus05, which dies at E 8.5 with cardiovascular and neural tube defects [16]. [score:1]
[1 to 20 of 4 sentences]
[+] score: 7
Of these, miR-500-3p, miR-23b-3p, miR-200a-3p, miR-19b-3p, miR-92a-1-5p, miR-21-5p, miR-21-3p, miR-1843-3p, miR-223-3p, miR-3473, and miR-129-2-3p were found to be upregulated, whereas miR-92b-3p, miR-3102, and miR-3577 were found to be downregulated in the rat brain. [score:7]
[1 to 20 of 1 sentences]
[+] score: 7
Similarly, analysis of miRNA profiles of hippocampal neurons during I/R injury revealed that hydrogen inhibits I/R -induced expression of the miR-200 family by reducing ROS production, which has led to suppression of cell death [94]. [score:7]
[1 to 20 of 1 sentences]
[+] score: 7
miR-448, let-7b, miR-540, miR-296, miR-880, miR-200a, miR-500, miR-10b, miR-336, miR-30d, miR-208, let-7e, miR-142-5p, miR-874, miR-375, miR-879, miR-501, and miR-188 were upregulated, while miR-301b, miR-134, and miR-652 were downregulated in TMH group (Table 5). [score:7]
[1 to 20 of 1 sentences]
[+] score: 6
Notably, our very recent data obtained in the R-H mo del showed that activation of NRF2/KEAP1 pathway, due either to down-regulation of miRNA-200a, which targets KEAP1, or to extremely frequent missense mutations of NRF2, characterizes preneoplastic nodules and persists all throughout the process up to HCC development [48]. [score:6]
[1 to 20 of 1 sentences]
[+] score: 6
Current studies on diabetic processes indicate that miRNA-216, miRNA-217, and miRNA-21 target PTEN [6], and the miRNA-200 family targets friend of GATA (FOG)2 [32] to activate the Akt/mTOR signaling pathway, thereby mediating DN occurrence and development. [score:6]
[1 to 20 of 1 sentences]
[+] score: 6
Dysregulated miR-124 and miR-200 expression contribute to cholangiocyte proliferation in the cholestatic liver by targeting IL-6/STAT3 signalling. [score:6]
[1 to 20 of 1 sentences]
[+] score: 5
In serum exosomes, a total of 962 targets of rno-miR-145-3p, rno-miR-181a-5p, rno-miR-21-5p, rno-miR-200a-5p, rno-miR- 375-3p, and rno-miR-1b were predicted by Target Scan, miRDB, and DIANA Tools. [score:5]
[1 to 20 of 1 sentences]
[+] score: 5
The involvement of miRNAs, such as the miR-200 family members (miR-200a, miR-200b, miR-200c, miR-141, and miR-429), regulating EMT has been shown earlier; in addition, their dysregulated expression was described in several oncologic conditions [11, 12]. [score:5]
[1 to 20 of 1 sentences]
[+] 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-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, 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-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-211, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
We used TargetScan and miRanda database queries to obtain miRNAs, which had higher targeting combined with N4bp2, namely, miR-200, miR-429, miR-29 and miR-30. [score:5]
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[+] score: 4
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-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-32, hsa-mir-33a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-106a, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-9-2, mmu-mir-135a-1, mmu-mir-137, mmu-mir-140, mmu-mir-150, mmu-mir-155, mmu-mir-24-1, mmu-mir-193a, mmu-mir-194-1, mmu-mir-204, mmu-mir-205, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-143, mmu-mir-30e, hsa-mir-34a, hsa-mir-204, hsa-mir-205, hsa-mir-222, mmu-let-7d, mmu-mir-106a, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-137, hsa-mir-140, hsa-mir-143, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-150, hsa-mir-193a, hsa-mir-194-1, 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-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-23a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-92a-2, mmu-mir-34a, rno-mir-322-1, mmu-mir-322, rno-let-7d, rno-mir-329, mmu-mir-329, rno-mir-140, rno-mir-350-1, mmu-mir-350, hsa-mir-200c, hsa-mir-155, mmu-mir-17, mmu-mir-25, mmu-mir-32, mmu-mir-200c, mmu-mir-33, mmu-mir-222, mmu-mir-135a-2, mmu-mir-19b-1, mmu-mir-92a-1, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-7b, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-106b, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-375, mmu-mir-375, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-7b, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-17-1, rno-mir-19b-1, rno-mir-19b-2, rno-mir-23a, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-27b, rno-mir-29a, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-32, rno-mir-33, rno-mir-34a, rno-mir-92a-1, rno-mir-92a-2, rno-mir-106b, rno-mir-126a, rno-mir-135a, rno-mir-137, rno-mir-143, rno-mir-150, rno-mir-193a, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-204, rno-mir-205, rno-mir-222, hsa-mir-196b, mmu-mir-196b, rno-mir-196b-1, mmu-mir-410, hsa-mir-329-1, hsa-mir-329-2, mmu-mir-470, hsa-mir-410, hsa-mir-486-1, hsa-mir-499a, rno-mir-133b, mmu-mir-486a, hsa-mir-33b, rno-mir-499, mmu-mir-499, mmu-mir-467d, hsa-mir-891a, hsa-mir-892a, hsa-mir-890, hsa-mir-891b, hsa-mir-888, hsa-mir-892b, rno-mir-17-2, rno-mir-375, rno-mir-410, mmu-mir-486b, rno-mir-31b, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-499b, mmu-let-7j, mmu-mir-30f, mmu-let-7k, hsa-mir-486-2, mmu-mir-126b, rno-mir-155, rno-let-7g, rno-mir-15a, rno-mir-196b-2, rno-mir-322-2, rno-mir-350-2, rno-mir-486, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The prospect that a similar function may extend to other miRNAs is suggested by the conservation of several miRNAs (e. g. miR-25, miR-34a/b/c, miR-135a/b, miR-194, and miR-200a) that are capable of directly targeting the Wnt/β-catenin, a signaling pathway that has been wi dely implicated in the control of oncogenic hallmarks such as cell proliferation, metastasis, angiogenesis, telomerase activity, and apoptosis (reviewed by [49]). [score:4]
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[+] score: 4
Murakami et al. reported that 11 miRNAs including miR-34, miR-199a-5p, miR-199, miR-200, and let-7e were up-regulated in a CCl [4] -induced fibrosis mo del mouse [31]. [score:4]
[1 to 20 of 1 sentences]
[+] score: 4
miR-200a was shown to inhibit EMT and renal fibrosis in a TGF-β -induced diabetic kidney mo del [45]. [score:3]
The roles of miR-200 family in EMT and fibrogenesis have been well defined by previous research [43, 44]. [score:1]
[1 to 20 of 2 sentences]
[+] score: 4
Other miRNAs from this paper: rno-mir-200c, rno-mir-200b, rno-mir-429
However as Isopyrazam, unlike Sedaxane and Benzovindiflupyr, also caused a dose -dependent induction of miR200a and miR429, the effects of the SDHIs on all three miR 200a/22b/429 cluster members is concordant with its increased potency relative to Sedaxane at the level of hepatocellular tumours. [score:1]
In tumours the transcriptional repressor ZEB1 has been found to repress miRs 200a 200b and 429 [[19], [20]] that are thought to function to maintain epithelial differentiation, and ZEB1 and miR200 are interconnected via a double negative feedback loop [21]. [score:1]
At present there is no published data indicating whether or not CAR activator compounds will induce miR200a/200b/429 cluster members in mice. [score:1]
There was no change in either miR200a or miR 429 following Sedaxane treatment, (Fig. 2). [score:1]
[1 to 20 of 4 sentences]
[+] score: 4
miR-141, miR-200a, miR-192, and miR-205 are upregulated in patients with hypertensive glomerulosclerosis [43]. [score:4]
[1 to 20 of 1 sentences]
[+] score: 3
A previous study demonstrates that signal transducers and activators of transcription 3 (STAT3)-coordinated Lin-28-let-7-HMGA2 and miR-200-ZEB1 circuits initiate and maintain oncostatin M -driven EMT 5. The interplay of these EMT activators, such as HMGA2 and ZEB1 6– 8, represses E-cadherin expression. [score:3]
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[+] score: 3
[12] We showed that the inhibition of the miR-200 family and/or miR-182 family in SHSY5Y cells increased global protein conjugation by the abovementioned ULMs, and in so doing made these cells more resistant to OGD -induced cell death. [score:3]
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[+] score: 3
By contrast, miR-26b-5p, miR-199a-3p, miR-377–3p, miR-let-7f-5p, miR-200a-3p, miR-21–5p, miR-152–3p, and miR-192–5p expressions were repressed by SO diet consumption. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
By individual TaqMan qRT-PCR analysis of dysregulated serum miRNAs uncovered by serum TLDA and dysregulated liver tissue miRNAs uncovered by microarray hybridization in primary screening, 6 serum miRNAs, including miR-122, miR-192, miR-193, miR-200a, miR-21 and miR-29c, exhibited a high correlation with primary screening results. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
There were 8 miRNAs with fold changes in expression greater than 3 [miR-490-5p (FC = 9.44), miR-547-3p (FC = 4.77), miR-24-1-5p (FC = 3.78), miR-200a-5p (FC = 3.55), miR-139-3p (FC = 3.51), miR-139-5p (FC = 3.46), miR-676 (FC = 3.32), and miR-532-3p (FC = 3.07)]. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
Other miRNAs from this paper: rno-mir-200c, rno-mir-200b
Progesterone-activated genomic pathways could limit the expression of contractile agonists (e. g. oxytocin), receptors (e. g. prostaglandin receptors), contraction -associated protein (e. g. gap junctions), or microRNAs (e. g. miR-200 family) within the myometrium, and in turn cause long-term modulation of the uterine contractile phenotype [5, 18– 20]. [score:3]
[1 to 20 of 1 sentences]
[+] score: 3
Moreover, altered expressions of miR-18a, miR-124, miR-343-3p, miR-16, miR-141, miR-182, and miR-200a in the brain tissue of suicidal patients have been reported [6]. [score:3]
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[+] score: 3
However, there were striking differences in the expression of miRNAs such as miR-135a, miR-429, miR-200a/b and miR-215 which were not detected in our samples but were reported to be significantly decreased by Zhao et al [38]. [score:3]
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[+] score: 3
Many of the best-studied miRNAs contained TFBS (e. g., mir-200a, b, c; mir-125a; let-7b), including those that have wide tissue expression patterns (e. g. mir-16-2) and others enriched in specific organs such as brain (mir-124-1,2) or liver (mir-122) [7]. [score:3]
[1 to 20 of 1 sentences]
[+] score: 2
Other miRNAs from this paper: rno-mir-200c, rno-mir-200b
A potential regulator of the actomyosin system in TM cells is the miR-200 family. [score:2]
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In zebrafish the miRNAs are detected in the eye, nasal epithelium, and sensory hair cells of the ear and neuromasts [26], and injection of miR-183 and miR-200 family members into zebrafish embryos have been demonstrated to impact development and affect neuromast migration [28]. [score:2]
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Other miRNAs from this paper: rno-mir-127, rno-mir-200c, rno-mir-200b, rno-mir-210
Other components of cell-cell adhesion structures such as E-cadherin are also regulated by miRNAs, in particular, miR-200 family. [score:2]
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These exceptions are shown in Table 3 and include, among others, the β catenin-related miR-200a and the cell-cycle regulator miR-663. [score:2]
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MiR-200a can repress TGF-β2 expression to prevent renal fibrogenesis [17]. [score:2]
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Other miRNAs from this paper: rno-mir-27a, rno-mir-130b, rno-mir-146a, rno-mir-182
23, 32, 33 Several miRNAs, such as microRNA-130b, [34] microRNA-182, [35] microRNA-146a [36] and microRNA-200a, [37] have been found dysregulated in diabetes. [score:2]
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There are 5 and 3 nucleotide differences between miR-200c, and miR-200a and miR-200b, respectively. [score:1]
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A number of miRNAs have been shown to be relevant to fibrotic processes in diabetic nephropathy, including miR-29 and miR-200 families, miR-192 and miR-21 [14– 17]. [score:1]
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We selected the top 9 miRNAs (miR-200a, miR-200b, miR-182, miR-429, miR-183, miR-200c, miR-141, miR-96 and miR-24) showing the highest standard deviations. [score:1]
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MiR-200b belongs to the miR-200 family, which is organized into two groups based on a single nucleotide difference in their seed sequence (group A: miR-141 and -200a; group B: miR-200b, -200c and −429) [33]. [score:1]
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Accumulated evidence revealed that Keap1 was controlled by microRNAs, such as miR-200, miR-141 and miR-28 [16]. [score:1]
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A number of miRNAs have been identified to be involved in cardiac cell survival and death, such as miR-155, miR-874 and miR-200a-5p 8– 10. [score:1]
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Other miRNAs from this paper: rno-mir-34a, rno-mir-122, rno-mir-200b
miRNA results were examined in more detail by qRT-PCR for miR-34a and three other miRNAs (miR-122 and miR-200a/b) that were perturbed by 30 mg/kg bw/day furan treatment over 3 months in male Sprague- Dawley (SD) rats in another study (Chen et al. 2012). [score:1]
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The presence of miR-200 within the 3′-UTR of the human IDS gene was of special interest due to this miR family being induced and having a specific role during the late stages of neuronal differentiation (Beclin et al. 2016). [score:1]
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