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46 publications mentioning mmu-mir-148b

Open access articles that are associated with the species Mus musculus and mention the gene name mir-148b. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 265
Subsequent experiments confirmed that the cholecystokinin-B receptor (CCKBR) was a target of miR-148b and was down-regulated by miR-148b at the translational level. [score:8]
These results highlight that miR-148b interacts with CCKBR and negatively regulates its expression at the translational level. [score:6]
After Expression Analysis Systematic Explorer (EASE) analysis, eleven genes were picked out as candidate targets of miR-148b (Additional file 1 Table S4). [score:5]
These findings provide important evidence that miR-148b targets CCKBR and is significant in suppressing gastric cancer cell growth. [score:5]
Compared with GES-1, miR-148b was down-regulated with different expression levels in MGC-803 (0.21 ± 0.04-fold), SGC-7901 (0.34 ± 0.15-fold), BGC-823 (0.55 ± 0.21-fold) and AGS (0.79 ± 0.14-fold; Figure 1B). [score:5]
MiR-148b inhibits cell proliferation in vitroThe significant reduction of miR-148b expression in gastric cancer samples prompted us to explore the possible biological significance of miR-148b in tumorigenesis. [score:5]
Duursma et al. studied the target of miR-148 in the protein coding region and found that human miR-148 represses the expression of the DNA methyltransferase 3b (Dnmt3b) gene, which is the primary mediator of establishment and maintenance of DNA methylation in mammals [22]. [score:5]
Further investigation revealed that in gastric cancer cell lines, miR-148b functioned as a tumor suppressor and overexpression of miR-148b could inhibit cell proliferation in vitro and in vivo. [score:5]
This was further supported by the finding that the overexpression of miR-148b could inhibit tumor formation and growth in nude mice. [score:5]
The results above showed that miR-148b could inhibit cell proliferation in vitro and suppress tumorigenicity in vivo. [score:5]
Possibly, miR-148b regulates the expression of CCKBR depending on other binding sites or three-dimensional reconstructions of 3'UTR. [score:4]
Therefore, we propose that miR-148b may have an effect on proliferation in gastric cancer, depending on regulating the expression of CCKBR. [score:4]
Nevertheless, although down-regulation of miR-148b was detected in some cancers, only Zhao et al. found miR-148b may have a relationship with metastasis in hepatocellular carcinoma [21]. [score:4]
Therefore, miR-148b may regulate different targets in the same cells, in different cells or depending on different binding regions. [score:4]
Moreover, the expression of miR-148b was demonstrated to be associated with tumor size (P = 0.027) by a Mann-Whitney U test. [score:3]
Table S4: Putative target genes of miR-148b. [score:3]
After we quantified the protein fragments, an obvious inverse correlation was observed between the expression of CCKBR and miR-148b in tissue samples (P = 0.002, Table 2). [score:3]
Moreover, although CCKBR can be regulated by miR-148b, an indirect mechanism cannot be excluded. [score:3]
The anti-miR-148b, with sequence of 5'-ACAAAGUUCUGUGAUGCACUGA-3', was a 2'-O-methyl -modified oligoribonucleotide designed as an inhibitor of miR-148b. [score:3]
Moreover, an obvious inverse correlation was observed between the expression of CCKBR protein and miR-148b in 49 pairs of tissues (P = 0.002, Spearman's correlation). [score:3]
Many putative miR-148b targets are predicted by various computer-aided algorithms. [score:3]
However, in the present study, miR-148b expression was found to be associated with tumor size (P = 0.027) in gastric cancer patients. [score:3]
The relative expression ratio of miR-148b was presented as the fold change normalized to an endogenous reference (U6 RNA) and relative to the nontumorous controls (normal tissues and normal cell line). [score:3]
And subsequently, an obvious inverse correlation was observed between the expression of CCKBR and miR-148b in 49 pairs of tissue samples. [score:3]
Possibly the process of cell cycle arrest induced by miR-148b is influenced by another molecular mechanism as indirect regulation. [score:3]
Obviously, CCKBR protein levels were suppressed by miR-148b mimics in MGC-803 cells (Figure 4C). [score:3]
Although aberrant expression of miR-148b has been observed in several types of cancer, its pathophysiologic role and relevance to tumorigenesis are still largely unknown. [score:3]
To confirm CCKBR is a target of miR-148b, we transfected MGC-803 cells with miR-148b mimics and the NC. [score:3]
Figure 4 CCKBR is a potential target of miR-148b in SGC-7901, MGC-803, BGC-823 cells. [score:3]
The significant reduction of miR-148b expression in gastric cancer samples prompted us to explore the possible biological significance of miR-148b in tumorigenesis. [score:3]
Images were overlay images with brown color representing miR-148b expression. [score:3]
MiR-148b is located at chromosome 12q13 and recent studies have found it is down-regulated in oral, pancreatic, colon and gastric cancer tissues using microarray analysis [15- 18]. [score:3]
The purpose of this study was to elucidate the molecular mechanisms by which miR-148b acts as a tumor suppressor in gastric cancer. [score:3]
Taken together, these results suggest that reduced miR-148b is a frequent event in human gastric cancer tissues and may be involved in carcinogenesis as a tumor suppressor gene. [score:3]
We showed significant down-regulation of miR-148b in 106 gastric cancer tissues and four gastric cancer cell lines, compared with their non-tumor counterparts by real-time RT-PCR. [score:3]
These results indicate that CCKBR may be a target of miR-148b. [score:3]
Images are overlay images with brown color representing miR-148b expression. [score:3]
The patients with low expression of miR-148b tended to have larger tumor sizes (≥6 cm). [score:3]
An experiment in nude mice revealed that miR-148b could suppress tumorigenicity in vivo. [score:3]
Figure 1 The expression of miR-148b in tissues and cell lines. [score:3]
Maybe miR-148b would become a potential biomarker and therapeutic target against gastric cancer. [score:3]
In our study, we found significant low -expression of miR-148b in gastric cancer tissues and cell lines. [score:3]
The inverse correlation between the expression of miR-148b and CCKBR protein in cells and tissue samples. [score:3]
Furthermore, although we found an obvious inverse correlation between the expression of CCKBR and miR-148b in tissue samples, the correlation coefficient was not perfect (r = -0.436). [score:3]
To provide further evidence that miR-148b was indeed involved in gastric cancer cell growth, we studied the effect of the inhibitor of miR-148b in AGS cells. [score:3]
The Mann-Whitney U test revealed that the expression levels of miR-148b were associated with tumor size (P = 0.027) in gastric cancer patients (Table 1). [score:3]
On the other hand, what is responsible for miR-148b induced inhibition of proliferation? [score:3]
As an initial step, we detected expression of miR-148b by qRT-PCR 48 h after transfection of miR-148b mimics, anti-miR-148b, their respective NCs and blank controls (MGC-803). [score:3]
Our data also suggest that miR-148b can inhibit cell proliferation in vitro and in vivo. [score:3]
Moreover, the expression of miR-148b was found to be associated with tumor size in gastric cancer patients. [score:3]
To determine whether the inhibition of growth induced by miR-148b in cells was anchorage-independent, the cells were plated on soft agar 24 h after RNA transfection in SGC-7901 cells. [score:3]
The results revealed that the relative luciferase activity of the pGL3-CCKBR-3'UTR reporter was obviously suppressed by miR-148b mimics in these cells but pGL3-CCKBR-3'UTR-conserved or pGL3-CCKBR-3'UTR-poorly conserved had no overt variation (Figure 4B). [score:3]
However, the regulation processes of miR-148b, as well as the relationship between miR-148a, miR-148b and miR-152, need further study. [score:2]
In conclusion, we showed there was significant low -expression of miR-148b in gastric cancer tissues and cell lines compared with their non-tumor counterparts. [score:2]
CCKBR is a potential target of miR-148b in MGC-803, SGC-7901 and BGC-823 cells using a luciferase activity assay. [score:2]
Therefore, miR-148a, miR-148b and miR-152 may play the same role in gastric cancer by regulating the same targets, and the relationship among them need further investigation. [score:2]
In this study, we analyzed miR-148b expression in human gastric cancer tissues and their matched non-tumor adjacent tissues by both qRT-PCR assay and in situ hybridization. [score:2]
Our MTT assay and growth curves results both indicate that miR-148b is associated with significant growth inhibition in gastric cancer cells at different degrees. [score:2]
Interestingly, a recent study showed that the coding sequence of DNA methyltransferase 3b (Dnmt3b) mediated regulation by the miR-148 family (miR-148a and miR-148b) [22]. [score:2]
MiR-148b suppresses tumorigenicity in vivoTo confirm the above findings, an in vivo tumor mo del was used. [score:2]
Using a luciferase activity assay and western blot, CCKBR was identified as a target of miR-148b in cells. [score:2]
MiR-148b inhibits cell proliferation in vitro. [score:2]
MiR-148b suppresses tumorigenicity in vivo. [score:2]
Moreover, we used a luciferase activity assay and western blot to confirm that CCKBR is a target of miR-148b in cells. [score:2]
According to the results of the MTT assay and growth curves, we found that the cells (MGC-803, SGC-7901 and BGC-823), which were transiently transfected with miR-148b mimics, had a significant growth inhibition at different degrees (Figure 2A, B). [score:2]
Thus, the identification of the function of miR-148b is critical to understanding the role of miR-148b in cancer development. [score:2]
A, The relative expression of miR-148b which was transfected with miR-148b mimics was very high (476.33 ± 52.97-fold, compared with NC). [score:2]
B, The relative expression of miR-148b which was transfected with anti-miR-148b was significantly low (0.66 ± 0.55-fold, compared with anti-NC). [score:2]
Interestingly, the relative luciferase activity of these reporters was suppressed at different degrees when miR-148b mimics was cotransfected in MGC-803 cells compared with the NC (Figure 4A). [score:2]
Moreover, CCKBR is a potential target of miR-148b using a luciferase activity assay. [score:2]
It is worth considering whether there are other mechanisms involved in the regulation processes of miR-148b. [score:2]
Moreover, bioinformatics shows that miR-148b has the same "seed sequences" as miR-148a and miR-152, however, its pathophysiologic role and relevance to tumorigenesis are still largely unknown. [score:1]
Therefore, we used real-time PCR and in situ hybridization to profile the expression of miR-148b in a large number of cases and clarified the relationship between miR-148b and clinicopathological characteristics in gastric cancer. [score:1]
In cell lines, we investigated the expression level of miR-148b in gastric cancer cell lines (MGC-803, SGC-7901, BGC-823 and AGS) relative to the normal gastric epithelial cell line (GES-1). [score:1]
Indeed, our subsequent cell cycle analysis revealed that MGC-803 and SGC-7901 cells transfected with miR-148b mimics had an obvious cell cycle arrest at the S-G2/M phase. [score:1]
In situ detection of miR-148b was performed on paraffin sections using a DIG-labeled miRCURY™ Detection probe according to the manufacturer's instructions (Exiqon). [score:1]
In addition, we measured CCKBR protein levels in 49 pairs of the previously studied 106 gastric cancer tissues and their matched non-tumor adjacent tissues, which had already been verified as expressing miR-148b by qRT-PCR. [score:1]
Interestingly, miR-148b has the same "seed sequences" as miR-148a and miR-152. [score:1]
Among 106 patients with gastric cancer, 66 of 106 (62.26%) cases revealed >50% reduction in the miR-148b level relative to their matched non-tumor adjacent tissues (Figure 1A). [score:1]
Four weeks after injection, the group with miR-148b mimics had a lower mortality rate (9.09%) and formed substantially smaller tumors than the other 2 groups (Figure 3A). [score:1]
After four weeks, the cells transfected with miR-148b mimics formed significantly fewer colonies on soft agar than cells transfected with NC and the blank control (Figure 2D). [score:1]
One was pGL3-CCKBR-3'UTR-conserved, which contains a putative miR-148b binding site in a conserved region of 3'UTR (1904-2044 nt). [score:1]
Using a qRT-PCR method, miR-148b was detected in all 106 (100%) pairs of gastric cancer tissues and their matched non-tumor adjacent tissues, as well as the gastric cell lines. [score:1]
The results revealed that MGC-803 and SGC-7901 cells transfected with miR-148b mimics had an obvious cell cycle arrest at the S-G2/M phase (Figure 2E). [score:1]
Furthermore, with in situ hybridization of ten cases, miR-148b was detected both in the normal epithelial cells and in the carcinoma cells (Figure 1C). [score:1]
The statistical significance of correlations between the expression of miR-148b and CCKBR protein were calculated by a chi-square test and Spearman's rank correlation. [score:1]
This also indicates that miR-148b may play different roles in different cells. [score:1]
Moreover, some studies revealed that miR-148b may play a critical role in osteogenesis [19] and may influence the polymorphism of HLA-G [20]. [score:1]
In situ detection of miR-148b was performed on paraffin sections using DIG-labeled miRCURY™ Detection probe according to the manufacture's instructions (Exiqon). [score:1]
In addition, we also constructed a luciferase reporter that had a complete complementary sequence to miR-148b as a positive control (PC). [score:1]
48 h after transfection, the efficiency of transfection with miR-148b mimics or anti-miR-148b was monitored by qRT-PCR. [score:1]
Expression of miR-148b and its correlation with clinicopathological characteristics of gastric cancer. [score:1]
Table S2: The sequence of hsa-miR-148b mimics and negative control(NC), anti-miR-148b and anti-NC, siRNA and NC for CCKBR. [score:1]
Furthermore, Zhao et al. found miR-148b may play a role in metastasis related to hepatocellular carcinoma [21]. [score:1]
As shown on the miRbase website, miR-148a, miR-148b and miR-152 have the same "seed sequences". [score:1]
The tumor volume at the time of death in mice injected with miR-148b mimics -transfected cells was 60.49 ± 53.29 mm [3], whereas the tumor volume of mice injected with NC or MGC-803 cells were 140.81 ± 72.21 mm [3 ]and 180.43 ± 127.89 mm [3], respectively (Figure 3B). [score:1]
We then studied the correlation between miR-148b expression and clinicopathological characteristics of gastric cancer. [score:1]
In situ hybridization of ten cases confirmed an overt decrease in the level of miR-148b in gastric cancer tissues. [score:1]
Group 1 (miR-148b mimics) was injected with MGC-803 cells transfected with miR-148b mimics; group 2 (NC) was injected with MGC-803 cells transfected with NC; and group 3 (MGC-803) was injected with MGC-803 cells alone. [score:1]
Interestingly, luciferase reporters, pGL3-CCKBR-3'UTR-conserved and pGL3-CCKBR-3'UTR-poorly conserved, which have presumed sites, did not show a significant correlation with miR-148b. [score:1]
NM_176875) containing the putative miR-148b binding sites was amplified and cloned into the vector pGL3-control. [score:1]
The cases below the line (log2 = -1) revealed >50% reduction in the miR-148b level. [score:1]
The other was pGL3-CCKBR-3'UTR-poorly conserved, which contains a putative miR-148b binding site in a poorly conserved region of 3'UTR (1568-1753 nt). [score:1]
MiR-148b mimics -transfected MGC-803 cells (miR-148b mimics), NC -transfected MGC-803 cells (NC) and MGC-803 cells were injected separately into three groups of nude mice (n = 11). [score:1]
The anti-NC, with a sequence of 5'-CAGUACUUUUGUGUAGUACAA-3', was used as a negative control for anti-miR-148b in the antagonism experiment. [score:1]
In situ hybridization In situ detection of miR-148b was performed on paraffin sections using a DIG-labeled miRCURY™ Detection probe according to the manufacturer's instructions (Exiqon). [score:1]
Then, we found that the 3'-UTR of CCKBR has two presumed sites in the conserved and poorly conserved regions that can bind with the seed region of miR-148b. [score:1]
In view of the above, we speculate that miR-148b may participate in gastric cancer progression. [score:1]
Despite the effect of miR-148b on CCKBR protein levels, no effect on the CCKBR mRNA level was detected by qRT-PCR (Figure 4D). [score:1]
Figure S2: Transfection efficiency of miR-148b mimics or anti-miR-148b and their respective NCs and blank controls. [score:1]
We also found that miR-148b could inhibit cell proliferation in vitro by MTT assay, growth curves and an anchorage-independent growth assay in MGC-803, SGC-7901, BGC-823 and AGS cells. [score:1]
However, most studies addressing the molecular mechanism of miR-148b in cellular transformation and tumorigenesis are still in an early stage. [score:1]
400 ng of luciferase reporter, 40 pmol (miR-148b mimics or NC) and 40 ng of pRL-TK were added in every well. [score:1]
However, miR-148b has no effect on the CCKBR mRNA level detected by qRT-PCR. [score:1]
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2
[+] score: 255
miR-148b directly targets the 3’-UTR of MLH1 and regulates its expression level in lung cancer cellsTo explore potential gene targets of miR-148b that may be involved in this effect, we examined for putative targets using miRNA target prediction programmes and MLH1 showed up as one of the hits that are most prevalent and this protein has been reported to play a role in regulating radioresistance in colon cancer cells [23]. [score:14]
In particular, miR-148b has been reported to be down-regulated in NSCLC and associated with poor survival [19] and it may function as a tumour suppressor in NSCLC by targeting carcinoembryonic antigen (CEA) [18]. [score:8]
To explore potential gene targets of miR-148b that may be involved in this effect, we examined for putative targets using miRNA target prediction programmes and MLH1 showed up as one of the hits that are most prevalent and this protein has been reported to play a role in regulating radioresistance in colon cancer cells [23]. [score:8]
Figure 3 miR-148b directly targets the 3’-UTR of MLH1 and regulate its expression level in lung cancer cells(A) The wild-type 3’-UTR of mammalian MLH1 mRNA contains a putative miR-148b -binding site. [score:7]
miR-148b mediates radiosensitivity through regulating MLH1 protein expressionTo determine the importance of MLH1 in the regulatory role of miR-148b in radioresistance, we ectopically express MLH1 in A549 cells transfected with miR-148b mimic (Figure 4A). [score:7]
Up-regulation of miR-148b decreases A549 cell radioresistance in vivoTo validate the regulatory role of miR-148b in radioresistance in vivo, we examined the effects of miR-148b inhibition on radioresistance of A549 cells using xenograft mouse mo del. [score:7]
miR-148b directly targets the 3’-UTR of MLH1 and regulate its expression level in lung cancer cells. [score:7]
Clonogenic survival assay showed that effective up-regulation or down-regulation of miR-148b significantly inhibited or promoted cell survival in A549 cells compared with control cells after exposure to 4 Gy of γ-radiation. [score:7]
miR-148b directly targets the 3’-UTR of MLH1 and regulates its expression level in lung cancer cells. [score:7]
Several reports have supported that miR-148b is down-regulated in many cancer types, including NSCLC and may function as a tumour suppressor [16– 18]. [score:6]
In the present study, we found that overexpression or inhibition of miR-148b could increase or decrease radiosensitivity in NSCLC cells by regulating DNA repair pathway (Figure 2). [score:6]
Figure 1 miR-148b expression is negatively related to radioresistance in lung cancer(A and C) Quantitative real-time PCR analysis of relative miR-148b expression in serum (A) and tissue (C) of lung cancer patients (n=20) and healthy controls (n=20). [score:5]
Importantly, expression of miR-148b mimic significantly inhibited tumour growth after IR exposure in A549 xenograft with resultant increased apoptotic cell death (Figure 5). [score:5]
Additionally, knockdown of MLH1 sensitized A549 cells to irradiation, phenocopying the effect of miR-148b down-regulation (Figure 4A). [score:5]
miR-148b expression is negatively related to radioresistance in lung cancerIn order to identify the miRNAs implicated in lung cancer radiosensitivity, was used to monitor their expression in A549 cells 48 h after radiation treatment. [score:5]
Figure 2 miR-148b modulates radiosensitivity in lung cancer cells(A) Quantitative real-time PCR analysis of relative miR-148b expression in A549 cells transfected with miR-148b mimic or miR-148b inhibitor. [score:5]
Up-regulation of miR-148b sensitized radioresistant NSCLC A549 cells to IR by interfering DDR through down -regulating MLH1 protein level. [score:5]
Taken together, these results demonstrate that miR-148b can directly regulate MLH1 expression level. [score:5]
miR-148b was selected as the target miRNA as it showed greatest fold change in expression before and after irradiation. [score:5]
Up-regulation of miR-148b has been observed in human endothelial cells after ionized radiation [21]. [score:4]
Figure 5Up-regulation of miR-148b decreases A549 cell radioresistance in vivo(A) Image of representative tumours from control or miR-148b mimic transfected A549 xenografts 3 weeks after exposure to 8 Gy of γ-radiation. [score:4]
Additionally, stable knockdown of MLH1 in A549 cells phenocopied the effect of miR-148b overexpression by sensitizing these cells to irradiation (Figures 4C and 4D). [score:4]
Recently, it has been shown that miR-148b can reverse cisplatin-resistance in NSCLC via down -regulating DNA (cytosine-5)-methyltransferase 1 (DNMT1) expression [20]. [score:4]
To verify MLH1 is a direct target of miR-148b, we cloned the 3’-UTR of MLH1 containing the single putative miR-148b -binding site downstream of the Renilla luciferase open reading frame. [score:4]
miR-148b modulates radiosensitivity in lung cancer cellsTo investigate whether miR-148b is involved in regulating radiosensitivity in lung cancer cells, we transfected miR-148b mimic or inhibitor into A549 cells which led to a significant increase or decrease in miR-148b expression (Figure 2A). [score:4]
Up-regulation of miR-148b decreases A549 cell radioresistance in vivo. [score:4]
To investigate whether miR-148b is involved in regulating radiosensitivity in lung cancer cells, we transfected miR-148b mimic or inhibitor into A549 cells which led to a significant increase or decrease in miR-148b expression (Figure 2A). [score:4]
Figure 4 miR-148b mediates radiosensitivity through regulating MLH1 protein expression(A) Western Blot analysis of MLH1 protein level in A549 cells transfected with control or miR-148b mimic or miR-148b plus MLH1 cDNA. [score:4]
Additionally, miR-148b has been shown to reverse cisplatin resistance in NSCLC and is up-regulated after IR exposure in human endothelial cells [20, 21]. [score:4]
Up-regulation of miR-148b decreases A549 cell radioresistance in vivo. [score:4]
Therefore, dysregulation of miR-148b expression may be associated with radioresistance in lung cancer. [score:4]
These results suggest that miR-148b exerts its radiosensitizing effects primarily through regulating MLH1 expression. [score:4]
Our results showed that miR-148b can directly bind to the 3’-UTR of MLH1 and manipulation of miR-148b expression affected MLH1 protein level (Figure 3). [score:4]
To determine the importance of MLH1 in the regulatory role of miR-148b in radioresistance, we ectopically express MLH1 in A549 cells transfected with miR-148b mimic (Figure 4A). [score:4]
To validate the regulatory role of miR-148b in radioresistance in vivo, we examined the effects of miR-148b inhibition on radioresistance of A549 cells using xenograft mouse mo del. [score:4]
miR-148b mediates radiosensitivity through regulating MLH1 protein expression. [score:4]
In the present study, we found that miR-148b was down-regulated in human NSCLC and radioresistant patient samples. [score:4]
On the other hand, co-transfection of miR-148b inhibitor with wild-type MLH1 3’-UTR reporter construct into A549 cells significantly induced relative luciferase activity which was reversed when the miR-148b -binding site was mutated (Figure 3C). [score:3]
Although transfection of miR-148b mimic reversed radioresistance, overexpression of MLH1 eliminated this sensitizing effect (Figure 4B). [score:3]
In addition, transfection of miR-148b mimic or inhibitor decreased and increased MLH1 protein level in A549 cells (Figure 3D). [score:3]
The results showed lower expression of miR-148b in tumour tissues than in normal tissues (Figures 1A and 1C). [score:3]
miR-148b expression was analysed in lung cancerous tissues and matched non-cancerous tissues as well as serum from 20 CRC patients. [score:3]
Aberrant expression of miR-148b has been found in many cancer types, including breast cancer, prostate cancer, lung cancer, etc. [score:3]
Overexpression of MLH1 reversed the radiosensitizing effects of miR-148b mimic (Figure 4B). [score:3]
As shown in Figures 5(A)– 5(C), transfection with miR-148b mimic significantly reduced tumour size, inhibited tumour growth and reduced tumour weight. [score:3]
Transfection of miR-148b inhibitor, miR-148b mimic and its non-specific control (Invitrogen) were performed according to the manual provided with the siPORTM NeoFXTM Transfection Agent (Ambion). [score:3]
miR-148b expression is negatively related to radioresistance in lung cancer. [score:3]
In the present study, we identified a panel of altered miRNAs in a radioresistant NSCLC cell line A549, after IR exposure and analysed the expression level of one of the top candidates, miR-148b in clinical human samples (Supplementary Figure S1). [score:3]
On the contrary, significantly fewer foci persisted 2 and 6 h after irradiation in cells transfected with miR-148b inhibitor (Figure 2C). [score:3]
A549 cells were transfected with reporters containing the wild-type or mutant form after transfection with control miRNA as well as miR-148b mimic or inhibitor respectively. [score:3]
A549 cells transfected with miR-148b mimic or inhibitor were irradiated with 2 Gy of γ-radiation, stained with γ-H2AX antibody at subsequent time intervals, and γ-H2AX foci were counted. [score:3]
We observed that miR-148b was down-regulated in both serum and tissues from NSCLC patients compared with healthy controls. [score:3]
Taken together, these results suggest that miR-148b can regulate radioresistance in vivo. [score:2]
These results suggest that MLH1 is required for the regulatory role of miR-148b in radioresistance. [score:2]
This suggests that miR-148b regulates radioresistance through mediating DNA damage repair (DDR). [score:2]
As shown in Figure 3(B), co-transfection of miR-148b precursor with wild-type MLH1 3’-UTR reporter construct significantly repressed relative luciferase activity whereas mutation of the miR-148b -binding site eliminated this effect in A549 cells (Figure 3B). [score:2]
Two hundred and fifty nanograms of pGL3 reporter vector carrying the WT or mutant miR-148b -binding site (see plasmid construct, Figure 3A), 25 ng of the phRL-SV40 control vector (Promega) and 100 nM miRNA precursors or scrambled sequence miRNA control (Ambion) were co -transfected into HEK293 cells in 24-well plates. [score:1]
Control or miR-148b mimic transfected A549 cells (2×10 [6] cells/injection) were subcutaneously injected into both flanks of 5 weeks old female nude mice group. [score:1]
miR-148b may represent a novel biomarker for the prediction of radiosensitivity in NSCLC. [score:1]
These observations suggest that miR-148b may serve as a potential predictive biomarker for radiotherapy in NSCLC. [score:1]
miR-148b modulates radiosensitivity in lung cancer cells. [score:1]
Student's t test was used to compare the difference between control and miR-148b mimic group. [score:1]
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3
[+] score: 160
P-values are: miR-148a expression in 501mel  = 0.0940 and in MeWo  = 0.0148. miR-148b expression in 501mel  = 0.0023 and in MeWo  = 0.0065. miR-152 expression in 501mel  = 0.0054 and in MeWo =  0.9316. [score:7]
When both binding sites were functional miR-148 downregulated reporter gene expression to 50–60% compared to expression from the vector alone in 501mel cells (p = 0.0140) (Fig. 3A). [score:7]
However, when the 148/152B binding site was mutated, miR-148 was no longer able to downregulate reporter gene expression (p = 0.3929). [score:6]
When the 148/152A binding site was mutated, miR-148 downregulated reporter gene expression to 47% (p = 0.0049). [score:6]
These results indicate that miR-148 is able to downregulate Mitf expression by binding to the 148/152B binding site. [score:6]
Expression of miR-152 in 501mel was 2.7 fold lower than in HEK293 cells and was much lower then the expression of miR-148a and miR-148b in all cell types (see Table 2). [score:5]
Higher endogenous expression in HEK293 cells might explain why transfected miR-148 had no effect on reporter gene expression in HEK293 cells, except at the highest concentration. [score:5]
miR-148 and affect expression of the endogenous MITF In order to test if these miRNAs affect the level of endogenous MITF mRNA in melanoma cells, we used qRT-PCR to determine MITF mRNA expression after transfecting MeWo melanoma cells with the miRNAs miR-124, and miR-148. [score:5]
Of these potential target genes, 66 are common targets of both and miR-148. [score:5]
The microRNAs and miR-148 have many other potential target genes according to online prediction programs (Targetscan). [score:5]
Simultaneous transfection with and miR-148 did not result in further effects on MITF expression as it reduced expression to 67% (Cp value 22.3, p = 0.0051), which is similar to the reduction seen with alone (Fig. 4A). [score:5]
miR-148 expression has been shown to be downregulated in tissue samples from undifferentiated gastric cancer compared to normal tissue [49]. [score:5]
Microarray analysis revealed that miR-148b is downregulated in early melanoma progression, although it was not confirmed using qRT-PCR [30]. [score:4]
Interestingly, the MITF protein has been shown to bind to the promoter of miR-148b that is shown there to have functional target site within the Mitf 3′UTR sequence [62]. [score:3]
Similarly, the effects of and miR-148 on endogenous MITF mRNAs are inhibited when MeWo cells were co -transfected with anti-miRNAs (Fig. 5B). [score:3]
0011574.g006 Figure 6. Expression of endogenous miRNAs miR-148a, miR-148b and miR-152 in HEK293, 501mel and MeWo cells. [score:3]
miR-148 affected reporter gene expression more significantly in 501mel cells. [score:3]
miR-148 has 536 conserved targets, with a total of 581 conserved sites and 134 poorly conserved sites. [score:3]
The mutations are shown in Fig. 1C and the primers used for mutagenesis in Table 1. There are two target sites for miR-148/152 in the mouse Mitf 3′UTR sequence. [score:3]
miR-148 and affect expression of the endogenous MITF. [score:3]
There are two target sites for miR-148/152 in the mouse Mitf 3′UTR sequence. [score:3]
Consistent with previous results, cells simultaneously transfected with the luciferase vector construct, the miR-148 and the anti-miR-148 showed that the anti-miR148 molecule effectively inhibited the effects of miR-148 (Fig. 5A). [score:3]
In 501mel cells, miR-148 had significant effects on expression of the mouseMitf-3′UTR-luciferase reporter (Fig. 2A). [score:3]
The mutations are shown in Fig. 1C and the primers used for mutagenesis in Table 1. There are two target sites for miR-148/152 in the mouse Mitf 3′UTR sequence. [score:3]
Role of the miR-148/152 target sites. [score:3]
This indicates a possible negative feedback loop where higher amounts of MITF would lead to more miR-148 expression which in turn adjusts MITF protein at desirable levels. [score:3]
Expression of endogenous miRNAs miR-148a, miR-148b and miR-152 in HEK293, 501mel and MeWo cells. [score:3]
In order to test if these miRNAs affect the level of endogenous MITF mRNA in melanoma cells, we used qRT-PCR to determine MITF mRNA expression after transfecting MeWo melanoma cells with the miRNAs miR-124, and miR-148. [score:3]
It has not been shown previously that miR-148 and/or miR-152 can target Mitf. [score:3]
The microRNAs miR-148a and miR-148b have similar expression levels in all the cell types tested. [score:3]
of anti-miR-148 and miR-148 simultaneously with the Mitf-3′UTR-luciferase vector inhibits the effect of miR-148. [score:3]
A. of anti-miR-148 and miR-148 simultaneously with the Mitf-3′UTR-luciferase vector inhibits the effect of miR-148. [score:3]
A. Expression of human MITF mRNA in MeWo cells transfected with miR-124,, miR-148 or and miR-148 combined. [score:3]
The effects of and miR-148 when transfected seperatly, are blocked when the cells are transfected with and miR-148 inhibitors. [score:3]
These results show that the and miR-148 have the same effects on expression of the endogenous MITF gene as seen using the luciferase reporter assay. [score:2]
In melanoma cells, Mitf is regulated by and miR-148/152. [score:2]
We show that and miR-148 negatively affect Mitf mRNA in melanoma cells through conserved binding sites in the 3′UTR sequence. [score:1]
Combining both and miR-148 did not result in added effects on endogenous MITF mRNA levels. [score:1]
anti-microRNA where purchased from Ambion and are the following: anti-miR-137 (Product ID: AM10513) and anti-miR-148 (Product ID: AM10263). [score:1]
A. The line indicates the 3′ UTR region of the mouse Mitf gene, including the coding region of exon 9. Potential binding sites for miR-27, miR-124/506, miR-25/32/92/363/367, miR-148/152, and miR-101/144 in the mMitf 3′UTR sequence are indicated below the line and potential PAS sites above. [score:1]
Black bars: miR-124/506 binding sites, dark grey bars: binding sites, light grey bars: miR-148/152 binding sites, white bars: miR-27, miR-25/32/92/363/367 and miR-101/144. [score:1]
In the case of one of the miR-148 binding site, 148/152A, only 4 bases were mutated as a clone with the fully mutated binding site was not generated successfully. [score:1]
miR-148/152 affects mMitf RNA in melanoma cells. [score:1]
We tested the effects of microRNAs which have conserved binding sites in the 3′UTR region of Mitf, including miR-27a (located at 229–235 in the mouse Mitf 3′UTR sequence), miR-25/32/92/363/367 (1491–1497), miR-101/144 (3023–3029), miR-124/506 (1639–1646) and miR-148/152 (1674–1680 and 2931–2937) (Fig. 1A and 1B). [score:1]
When the 148/152B binding sites were mutated, the effects of miR-148 were eliminated. [score:1]
The roles of and miR-148 were analysed further by mutating the binding sites in the mouseMitf-3′UTR-luciferase reporter construct. [score:1]
A. Effects of miR-148 on the mouseMitf-3′UTR-luciferase reporter when the potential binding sites are mutated. [score:1]
The 3′UTR sequences of Mitf in 11 vertebrate species all contain the two conserved miR-148/152 binding sites. [score:1]
miR-148/152 affects mMitf RNA in melanoma cellsTo test the functionality of the miRNA binding sites, the mouse Mitf 3′UTR sequence was cloned downstream of a luciferase reporter gene. [score:1]
When the cells were transfected with either, miR-148 or simultaneously with both and miR-148, MITF protein levels were reduced. [score:1]
B. analysis on MITF protein levels in MeWo cells, when transfected with miR-124,, miR-148 or and miR-148 combined. [score:1]
Similarly, hypermethylation of the miR-148, 124a3 and miR-152 genes was found in 34-86% of primary human breast cancer specimens [50]. [score:1]
miR-148 affected the reporter only when transfected at the highest concentration (1pmol) (Fig. 2B). [score:1]
and miR-148 both led to reduced levels of MITF mRNA and protein. [score:1]
miR-148 and miR-152. [score:1]
P-values are: Scramble  = 0.0396; miR-124 = 0.2228; = 0.0069; miR-148 = 0.0051;+148 = 0.0051. [score:1]
The p-values are; miR-neg  = 0.14 miR-148 = 0.007, miR-148+anti-miR-148 = 0.119. [score:1]
ND (1/9) ND (0/9) 34.69 (7/9) 37.39 (1/3) miR-124 34.37 (9/9) 34.73 (5/9) 35.09 (2/9) 32.68 (3/3) miR-506 35.19 (2/9) 34.73 (3/9) 32.87 (9/9) ND (0/9) miR-148a 27.90 (9/9) 28.29 (9/9) 28.82 (9/9) 33.12 (3/3) miR-148b 28.37 (9/9) 28.65 (9/9) 29.37 (9/9) 35.19 (1/3) miR-152 34.08 (9/9) 35.12 (9/9) 34.26 (9/9) 35.05 (2/3) miR-16 contr. [score:1]
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4
[+] score: 90
Other miRNAs from this paper: mmu-mir-152, mmu-mir-148a
We also showed that alcohol -induced upregulation of both miR-148 and miR-152 play a key role in downregulating their common targets Dnmt1 and Dnmt3b. [score:9]
Taken together, these results suggest that upregulation of both miR-148 and miR-152 plays a causal role in suppressing their common targets, Dnmt1 and Dnmt3b, in mice fed a liquid alcohol diet. [score:8]
miR-148 and miR-152, which target Dnmt1 and Dnmt3b, are upregulated in the livers of the wild type mice fed the liquid alcohol diet. [score:6]
Ethanol feeding caused pronounced decrease in hepatic Dnmtase activity in Dnmt1 [+/+] mice due to decrease in Dnmt1 and Dnmt3b protein levels and upregulation of miR-148 and miR-152 that target both Dnmt1 and Dnmt3b. [score:6]
miR-148 and miR-152 that Target Dnmt1 and Dnmt3b are Upregulated in the Livers of Mice Fed Alcohol Diet. [score:6]
These results suggest that co-ordinate upregulation of miR-148/152 is likely to be involved in down regulation of hepatic Dnmt1/3b in alcohol fed mice. [score:5]
The lack of inhibition of relative luciferase activity in cells transfected with the mutant psiCHECK2-Dnmt1-3′UTR vector lacking the miR-148/152 cognate site validated Dnmt1 as a true target of these two miRs. [score:5]
We focused on miR-148/152 because only these two miRs have a common site on Dnmt1 3′-UTR, which is conserved in mammals, and miR-148 and miR-152 have been previously shown to target Dnmt1 by interacting through its 3′-UTR [41], [42], whereas miR-148 targets Dnmt3b by binding to its cognate site in the coding region [36]. [score:5]
C. qRT-PCR analysis confirmed upregulation of hepatic miR-148&152 in mice fed alcohol. [score:4]
F. Endogenous DNMT1 and DNMT3b protein levels were reduced in cells expressing ectopic miR-148/152. [score:3]
Interestingly, miR-148 has been shown to target Dnmt3b by complementary base pairing with two conserved sites located in its coding region [36]. [score:3]
B. Northern blot analysis demonstrated increased expression of miR-148 in mice fed alcohol. [score:3]
0041949.g002 Figure 2 A. miR-148/152 cognate site predicted by TargetScan in the 3′-UTR of Dnmt1. [score:3]
E. Upregulation of miR-148/152 in Hepa cells transfected with the respective miRs compared to the controls (NC RNA transfected cells). [score:3]
D. Dnmt1 is a validated target of miR-148&152. [score:3]
A. miR-148/152 cognate site predicted by TargetScan in the 3′-UTR of Dnmt1. [score:3]
qRT-PCR analysis confirmed 40% increase in miR-148 level whereas miR-152 expression (not detectable by Northern blotting) increased by 85% in the livers from mice fed the liquid alcohol diet compared to controls (Figure 2C ). [score:2]
Relatively less pronounced inhibition of reporter activity in miR-148b transfected cells compared to those transfected with NC RNA is probably due to higher miR-148b level in these cells, which was elevated only 2 fold upon transfecting miR-148b mimic (Figure 2D, E ). [score:2]
After 48 h, cells were assayed for relative luciferase (renilla/firefly) activity and miR-148b/152 expression. [score:2]
We then investigated whether Dnmt1 is a target of miR-148 and/or miR-152. [score:1]
Hepa cells were transfected with psiCHECK2 vector harboring wild type or mutant Dnmt1 3′-UTR downstream of renilla luciferase coding region along with 50 nM miR-148b/152 mimic or scrambled RNA (NC RNA). [score:1]
The results showed that miR-148b and miR-152 could reduce Dnmt1 3′-UTR driven renilla luciferase (RLU2) activity by 20% and 45%, respectively (Figure 2D ). [score:1]
Next, we examined whether endogenous Dnmt1 and Dnmt3b protein level could be modulated by miR-148 and miR-152 by transfecting these miRs or respective NC RNAs into H293T cells. [score:1]
For this purpose, we cloned 3′-UTR of Dnmt1 into psiCHECK2 vector downstream of the renilla luciferase coding region and transfected it in Hepa cells along with miR-148b, miR-152 or negative control RNA (NC RNA). [score:1]
Total RNA (5 µg) was separated in 15% acrylamide-8 M urea gel, transferred to nylon membrane and subjected to Northern blotting using [32]P-labeted anti-miR-148 oligo as probe, washed and subjected to autoradiography. [score:1]
H293T cells obtained from ATCC, were transfected with 50 nM miR-148/152 mimic or NCRNA were harvested after 48 h and 72 h, harvested, and whole cell extracts prepared in cell lysis buffer were subjected to imunoblotting with Dnmt1,3a,3b and Gapdh antibodies. [score:1]
Briefly, growing Hepa (hepatoma) cells (1×10 [5] cells/well), obtained from ATCC, were plated in 24-well plates the day before and transfected with 100 ng of psiCKECK2 harboring Dnmt1 3′-UTR, together with 50 nM miR-148a (Sigma) or miR-148b (Invitrogen), miR-152 (Invitrogen) mimics or respective negative control RNAs (NCRNAs) (Sigma/Invitrogen). [score:1]
org/mmu_50/) [35] search revealed that 3′-UTR of Dnmt1 harbors only one conserved site for miR-148 and miR-152 (Figure 2A ). [score:1]
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5
[+] score: 30
Table 1 The role of miRNAs in autoimmune diseases miRNA Predicted/Identified targets Function Related diseases miR-22 IRF8Enhances CD11c [+]CD11b [+]B220 [−] cDC generation at the expense of pDCs miR-142 IRF8Plays a pivotal role in the maintenance of CD4 [+] DCs miR-142-3p IL-6 Specifically inhibits IL-6 expression by moDC MS miR-21 IL-12p35, Wnt1 Negatively regulates the production of IL-12 by moDC; negatively regulate the development of moDC SLE, IBD, UC, MS miR-10a IL-12/IL-23p40 Suppress the production of IL-12 and IL-23 by moDC SLE miR-148/152 Calcium/Calmodulin- dependent protein kinase IIa Suppress the production of IL-12 and IL-6 SLE miR-23b Notch1, NF-κB Inhibits the production of IL-12 while promotes IL-10 production UC miR-155 SOCS1, SHIP1, TAB2 Positively regulates the production of several pro-inflammatory cytokines including IL-6, IL-23, IL-12, and TNF-α RA, IBD miR-146a IRAK1, TRAF6 Negatively regulates TLR4-NF-κB pathway in monocytes RA, SLE, IBD miR-34a JAG1 Negatively regulates the development of moDC MS miR-223 C/EBPβNegatively regulates LCs -mediated antigen-specific CD8 [+] T cell proliferation, production of inflammatory cytokine TNFα, IL-1β, and IL-23 by intestinal DCs. [score:25]
For example, miR-148/152 suppressed IL-12 as well as IL-6 production; miR-23b suppressed IL-12 production while enhancing IL-10 production (Liu et al., 2010). [score:5]
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6
[+] score: 27
Pathways analysis predicted that miR-101a is targeting TGFBR1 and SMAD3, miR-582 is targeting TGFB2, SMAD1, miR-425 is targeting TGFBR2 and FST, miR-199a is targeting ACVR2a, miR-148 is targeting ACVR1, and miR-103 is targeting BMP2 in TGF- β signaling pathway. [score:13]
Predicted target and pathway analysis concluded that miR-101a is targeting TGFBR1 and SMAD3, miR-425 is targeting TGFBR2 and FST, miR-582 is targeting SMAD1 and TGFB2, miR-148 is targeting ACVR1, and miR-199a is targeting AcvR1a gene in the TGF- β signaling pathway. [score:13]
MiR-133a [23, 38], miR-378a [50], miR-26a [51], miR-27b [52, 53], miR-21a [56], miR-29a [44], miR-148 [58], and miR-103 are skeletal muscle specific miRNAs and play a vital role in muscle differentiation and proliferation as reported in previous studies. [score:1]
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7
[+] score: 25
However, miR-409-3p, Let-7i and miR-30c already exhibited a significant down-regulation while miR-148b was the only up-regulated miRNA in hippocampus at this age (Fig 3C). [score:7]
As mice approach 6-7 months of age they reach the critical period of Aβ-plaque formation and it was here that a significant down-regulation was seen in nearly all miRNAs tested including the previously up-regulated miR-148b (Fig 3D). [score:7]
A recent study by Nunez-Iglesias et al found forty-eight significantly deregulated miRNAs in human AD parietal lobe cortex, of which miR-148b, 20b and 181c were down-regulated [33]. [score:5]
The overlap between human AD and our in vitro and in vivo AD mo dels indicates that amongst the complex pathology in human AD brain, down-regulation of miR-9, miR-181c, miR-30c, miR-20b, miR-148b and Let-7i could be attributed at least in part to the presence of Aβ. [score:4]
Individual TaqMan assays (Applied Biosystems) were used to analyse the expression of the following mature mouse miRNAs: miR-181c, miR-9, miR-20b, miR-21, miR-30c, miR-148b, miR-361, miR-409-3p and Let-7i. [score:2]
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8
[+] score: 18
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-19a, hsa-mir-20a, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-33a, hsa-mir-96, hsa-mir-98, hsa-mir-103a-2, hsa-mir-103a-1, mmu-let-7g, mmu-let-7i, mmu-mir-23b, mmu-mir-30a, mmu-mir-30b, mmu-mir-99b, mmu-mir-125a, mmu-mir-125b-2, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-146a, mmu-mir-155, mmu-mir-182, mmu-mir-183, mmu-mir-24-1, mmu-mir-191, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-181b-1, hsa-mir-182, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-221, hsa-mir-223, hsa-mir-200b, mmu-mir-299a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-191, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-146a, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, 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-20a, mmu-mir-21a, mmu-mir-23a, mmu-mir-24-2, mmu-mir-26a-1, mmu-mir-96, mmu-mir-98, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-351, hsa-mir-200c, hsa-mir-155, hsa-mir-181b-2, mmu-mir-19a, mmu-mir-25, mmu-mir-200c, mmu-mir-223, mmu-mir-26a-2, mmu-mir-221, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-181b-1, mmu-mir-125b-1, hsa-mir-30c-1, hsa-mir-299, hsa-mir-99b, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-361, mmu-mir-361, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-375, mmu-mir-375, hsa-mir-148b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, mmu-mir-433, hsa-mir-429, mmu-mir-429, mmu-mir-365-2, hsa-mir-433, hsa-mir-490, hsa-mir-193b, hsa-mir-92b, mmu-mir-490, mmu-mir-193b, mmu-mir-92b, hsa-mir-103b-1, hsa-mir-103b-2, mmu-mir-299b, mmu-mir-133c, mmu-let-7j, mmu-mir-30f, mmu-let-7k, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
The reduction of Cxcr3, Fut1, and Rhobtb1 expression was associated with an increased expression of miR-148b, miR-125a, and miR-182, which target Cxcr3, Fut1, and Rhobtb1 mRNAs, respectively, suggesting that, in addition to Aicda and Prdm1, which are already downregulated by HDI, other genes can also be downregulated by HDI through upregulation of their targeting miRNAs. [score:18]
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9
[+] score: 18
Members of the miR-148 family (miR-148a, miR-148b, and miR-152) are upregulated upon DC stimulation by LPS, and their overexpression reduces MHC II expression on DC surface, inhibits the secretion of some proinflammatory cytokines, and reduces DC -mediated CD4 [+] T cell expansion. [score:10]
Correspondingly, MHC II expression, cytokine production, and CD4 [+] T cell proliferation increase when LPS-stimulated DCs are treated with miR-148 family inhibitors [35]. [score:5]
MicroRNAs regulate DC activation (let-7i, miR-142-3p, miR-146a, the miR-148 family, and miR-155), as well as cytokine production and development of DCs (miR-155) [28, 29]. [score:3]
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10
[+] score: 17
Other miRNAs from this paper: mmu-mir-148a
Indeed, enforced miR-148 expression inhibited the activity of these targets 3′UTR reporter vector in dual luciferase reporter assays, while mutation in miR-148a binding sites abrogated this repression; Suppression of miR-148a-3p and 5p using their respective sponge or inhibitor enhanced the activity of Pgc1 α, Sirt7 and HMGCR, YBX1 3′-UTR reporter vector in the same assays,respectively, while mutation in miR-148a-3p/5p -binding sites abrogated this upregulation (Figure 5c). [score:14]
Pparg co-activator 1 alpha (Pgc1 α), sirtuin 7 (Sirt7) and Hmgcr, Y-box binding protein 1 (Ybx1) which are involved in the processes of lipid metabolism and hepatocarcinogenesis were all identified as potential targets of miR-148-3p and 5p, respectively. [score:3]
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11
[+] score: 16
By analyzing regulation of miRNA expression in wild type cells and cells expressing a GR with impaired dimerization 11, we found several miRNAs up-regulated including let-7, miR-146a, miR-148a, miR-148b and miR-152 by GC treatment, some of them exclusively in wildtype cells, and not in GR [dim] cells. [score:9]
In the total pool of differentially expressed miRNAs in Dex -treated wild type and GR [dim] mesenchymal cells we found eight identical miRNAs that were up regulated (let-7a, let-7c, let-7f, let-7g, let-7i, miR-148a, miR-148b and miR-152) indicating GR monomer dependent GC regulation of miRNA expression (Table S1). [score:7]
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12
[+] score: 16
In the present study, we showed that the expression of several miRNAs is altered during the development of PC and that licofelone reverses the altered expression of the majority of these miRNAs with up-regulation of miR-21, miR-222, Let-7, miR-125, miR-142 and down-regulation of miR-1, miR-122 and miR-148. [score:12]
Most importantly, the miRNAs most strongly implicated in regulation of arachidonic acid metabolism via COX-2 and 5-LOX — like miR-199a, miR-21, miR-146, miR-29, miR148 — were tremendously modulated by licofelone treatment, clearly demonstrating targeted effects of this agent (Fig. 7C–7G, Supplementary Table 1). [score:4]
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13
[+] score: 16
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]
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]
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14
[+] score: 14
As shown in Figure 6, qualitative qPCR validated that ssc-miR-146a-5p, ssc-miR-221-5p and ssc-miR-148b-3p were significantly upregulated by LPS, and ssc-miR-215 and ssc-miR-192 were downregulated. [score:7]
After normalization of the raw reads we found that four miRNAs (ssc-miR-146a-5p, ssc-miR-221-5p, ssc-miR-9860-5p and ssc-miR-148b-3p) were significantly upregulated in the LPS-challenged samples with a p-value cutoff of 0.05. [score:4]
Differential expressions of five selected miRNAs (ssc-miR-146a-5p, ssc-miR-221-5p, ssc-miR-148b-3p, ssc-miR-215 and ssc-miR-192) were validated by quantitative polymerase chain reaction (qPCR). [score:3]
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15
[+] score: 12
It is worth to note that the observed liver detargeting effects will not only account from miR-148a binding to the inserted target sites but also from the recognition by all the miR-148/152 family members, since miR148a, miR-148b and miR-152 can recognize miR-148a target sites and downregulate transgenes with engineered target sites [8]. [score:12]
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[+] score: 10
We found that miR-152 expression, but not miR-148a and miR-148b expressions, was obviously increased by Sal B (Fig. 8A). [score:5]
Using the computer-aided algorithms, TargetScan, miRanda and miRDB, we predicted a group of miRNAs that have sequence complementarity to the 3′-UTR of DNMT1, namely miR-148a, miR-148b and miR-152. [score:3]
To detect miR-148a, miR-148b and miR-152 expression, the RT reaction was performed using the TaqMan MicroRNA Assay (Applied Biosystems, Foster City, CA, USA) according to the manufacturer's instructions. [score:2]
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[+] score: 9
Several human miRs, including miR-29 family, miR-148, and miR-200b/c have been found to be frequently downregulated in human cancers and lead to increase expression of DNMT1 and DNMT3a/b because they directly target the 3′-UTR of DNMTs [30, 35, 36]. [score:9]
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[+] score: 9
Further, p53 appears to regulate the expression of Dicer through its transcriptional target miRs, such as miR-192, 215, miR29a/b/c, miR-148, miR-15/16a, miR-206, and miR-103 [Table 2], suggesting that p53/p63/p73 could regulate the expression of dicer both at the transcriptional and the post-transcriptional level. [score:9]
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[+] score: 9
In the current study, we identified miR-148a as a suppressor of metastasis, particularly for TNBC, as its expression pattern is inversely correlated with tumor grade and metastatic potential, but directly correlated with prognosis of those patients since lower expression of miR-148 is associated with poor survival. [score:8]
Our previous results demonstrated that miR-148 does not strongly influence MDA-MB-231 cell-autonomous behaviors. [score:1]
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20
[+] score: 8
miR-148b, which is frequently down-regulated in gastric cancer, can suppress gastric cancer cell growth by targeting the cholecystokinin-B receptor [9]. [score:8]
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[+] score: 8
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 In order to understand the interaction between different genes, we generated common networks using Ingenuity Pathway Analysis (IPA) software. [score:4]
miR-148b −2.6183 decrease apoptosis miR-152 −2.3341 Increase cell growth miR-17 −6.2545 Bcl2, N-myc miR-181c −3.5756 proliferation and remo deling of muscles miR-190b −2.2 Binds to Ubiquitin-specific protease 46, increase cell growth miR-192 −2.4871 Increase cell growth miR-199a-3p −1.9 Activin receptor IIA, Map3k4 miR-218-1 −2.2887 Increase cell growth miR-23b −2.1623 Increase Cell growth, proliferation miR-26a −2.4565 decrease proapoptotic signaling miR-27a −2.7 Ubiquitin-conjugating enzyme E2N miR-27b −3 Ubiquitin-conjugating enzyme E2N miR-296-3p −7.3378 Increase cell growth, decrease apoptosis miR-322 8.7 Hydroxysteroid (17-beta) dehydrogenase 7 miR-455 129.249 Up-regulated brown adipocyte differentiation miR-470 3.2 TGFB -induced factor homeobox 1 miR-715 18.25 Fucosyltransferase 1 miR-7a −6.2174 Increase cell growth, decrease apoptosis miR-93 −48.423 Map3k14 (NIK) miR-98 1.8 Tripartite motif-containing 6, insulin-like growth factor 2 mRNA binding protein 1 A) C2C12 myotubes were treated with 10ng/ml of TWEAK for 18h following isolation of total RNA enriched with small RNAs. [score:4]
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These upregulated miRNAs include certain known miRNAs (mmu-miR-148b-5p, mmu-miR-879-5p, mmu-miR-144-3p, mmu-miR-540-5p, mmu-miR-582-5p, mmu-miR-15b-5p, mmu-miR-210-5p, mmu-miR-871-3p, mmu-miR-3103-5p, mmu-miR-16-1-3p, mmu-miR-470-5p, mmu-miR-190b-5p, mmu-miR-384-5p and mmu-miR-490-5p), as well as some novel miRNAs (novel_mir_46, novel_mir_214 and novel_mir_213) with their stem loop structures by Miredp (S3 Fig). [score:4]
Through sequencing miRNAs for their quantifications, we show that some known miRNAs (miR-148b-5p, miR-879-5p, miR-144-3p, miR-540-5p, miR-582-5p, miR-15b-5p, miR-210-5p, miR-871-3p, miR-3103-5p, miR-16-1-3p, miR-470-5p, miR-190b-5p, miR-384-5p and miR-490-5p) are upregulated in CUMS -induced depression mice (Table 3), which degrade mRNAs listed in Table 1. In other words, the analysis from miRNA sequencing is consistent to the analysis from mRNA sequencing. [score:4]
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Additionally, activation of repair -mediated DNA demethylation (Barreto et al. 2007) and decreased expression and/or functioning of Dnmt1 caused by a number of factors, including direct effects of BD and its metabolites on Dnmt1 protein, aberrant expression of microRNAs (e. g., miR-29b, miR-148, and miR-152), and expression of chromatin-modifying proteins (Garzon et al. 2009; Huang et al. 2010; Vire et al. 2006; Wang et al. 2009), may further contribute to the loss of DNA methylation. [score:8]
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Similarly, we found an increased expression of let-7i-5p, miR-29a-3p, miR-29c-3p, miR-30a-5p, miR-98-5p, miR-138-5p, miR-139-5p, miR-140-5p, miR-146b-5p, miR-148b-3p, miR-181a-1-3p, miR-181a-5p, miR-194-5p, and miR-342-3p, all of which have been reported to be altered in different AD tissues (Cogswell et al., 2008; Hebert et al., 2008; Maes et al., 2009; Wang et al., 2011, 2012; Lau et al., 2013). [score:3]
Interestingly, miR28a-5p, miR-98-5p, and miR-148b-3p expression was significantly higher in sedentary SAMP8 compared with sedentary SAMR1 mice and this difference was further accentuated by exercise (Figures 2A–C). [score:2]
We found that miR-28a-5p, miR-98a-5p, miR-148b-3p were altered in sedentary SAMP8 compared with SAMR1 mice and changed their expression levels in response to exercise (putative aging markers responsive to exercise). [score:2]
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In line with the known role of this drug to activate AMPK 4, considered an ideal drug target for cancer treatment 38, metformin upregulated both miR-148b, which targets this kinase, and miR-30b, belonging to a family of miRNAs that are known to modulate AMPK 39. [score:7]
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For example, miR-204 is primarily expressed in insulinomas and co-localizes mainly with insulin [43]; miR-127-3p and miR-184 are positively correlated with insulin biosynthesis and negatively correlated with glucose-stimulated insulin secretion (GSIS) [44]; miR-148 controls the insulin content in β-cells through regulation of the insulin repressor SOX6 [45] and miR-29 contributes to pancreatic β-cell dysfunction in prediabetic NOD Mice [46], and affects the release of insulin from β-cells by silencing of monocarboxylate transporter (MCT1) [47]. [score:4]
Indeed it has been reported that miR-24, miR-26 and miR-148 contribute to characterization of β-cell identity and maintenance of β-cell phenotype by suppressing two known insulin transcription repressors, Sox6 and Bhlhe22 [45]. [score:1]
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However, other studies have found little or no change in Wnt1 or Wnt10b expression by miR-148a or miR-148b in gastric cancer cells 38 39, suggesting that inhibition is dependent on cellular context. [score:5]
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Other miRNAs from this paper: hsa-mir-148b
Overexpression of miR-148b in melanoma cells significantly inhibited metastasis by reducing ITGa5 [49]. [score:5]
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miR-148b functions as a tumor suppressor in pancreatic cancer by targeting AMPKα1 [17]. [score:5]
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It is important to note that overlapping functions of miR-223 and miR-148b could be due to common target genes, in fact miR-148b shares four nucleotides of the seed region with miR-223. [score:3]
Relevantly, miR-223, like other microRNAs such as miR-31 [73], miR-148b [46] and miR-200bc [74], is involved in drug sensitivity, suggesting a potential function as adjuvant therapy, as recently reported also by [75], [76]. [score:1]
For instance, miR-31 and miR-148b control several steps of metastatization from anoikis to invasion and colonization [31], [46]. [score:1]
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MiR-148a and miR-148b, which are found in UC blood MSC-derived exosomes, reportedly regulate the proliferation of UC blood MSCs by upregulating NF-κB or hedgehog signalling [38]. [score:5]
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Three probesets aligned to regions that contain structural variants among CC founder strains (miR-148b, miR-192, and miR-194), but the observed patterns of expression were not correlated with the strain distribution of structural variants. [score:3]
We added miR-148b and miR-182 due to published evidence indicating roles in asthma or allergic inflammation in the lung [10, 26], and miR-17* and U6 for normalization. [score:1]
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Recently, deregulations of many miRs have been implicated in the growth and metastasis of HCC, such as miR-21 [11], miR-101 [12], miR-124 [13], miR-203 [13], and miR-148 [14], which may be used as potential therapeutic targets or candidates for HCC treatment. [score:4]
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In addition to mir-34a, p53 protein promotes the expression of other miRNAs in lung cancer cells, including mir-184, mir-148, and mir-181. [score:3]
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When comparing young versus aged TEC (a mix of cTEC and mTEC) a decrease in miR-148b, miR-19b, miR-24, and miR-322 expression was seen in aging (45). [score:3]
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Other miRNAs from this paper: hsa-let-7c, hsa-let-7d, hsa-mir-16-1, hsa-mir-21, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-28, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-99a, hsa-mir-101-1, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-30a, mmu-mir-99a, mmu-mir-101a, mmu-mir-125b-2, mmu-mir-126a, mmu-mir-128-1, mmu-mir-9-2, mmu-mir-142a, mmu-mir-144, mmu-mir-145a, mmu-mir-151, mmu-mir-152, mmu-mir-185, mmu-mir-186, mmu-mir-24-1, mmu-mir-203, mmu-mir-205, hsa-mir-148a, hsa-mir-34a, hsa-mir-203a, hsa-mir-205, hsa-mir-210, hsa-mir-221, mmu-mir-301a, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-125b-1, hsa-mir-128-1, hsa-mir-142, hsa-mir-144, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125b-2, hsa-mir-126, hsa-mir-185, hsa-mir-186, mmu-mir-148a, mmu-mir-200a, mmu-let-7c-1, mmu-let-7c-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-24-2, mmu-mir-29a, mmu-mir-31, mmu-mir-34a, mmu-mir-339, mmu-mir-101b, mmu-mir-28a, mmu-mir-210, mmu-mir-221, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-125b-1, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-200a, hsa-mir-101-2, hsa-mir-301a, hsa-mir-151a, hsa-mir-148b, hsa-mir-339, hsa-mir-335, mmu-mir-335, hsa-mir-449a, mmu-mir-449a, hsa-mir-450a-1, mmu-mir-450a-1, hsa-mir-486-1, hsa-mir-146b, hsa-mir-450a-2, hsa-mir-503, mmu-mir-486a, mmu-mir-542, mmu-mir-450a-2, mmu-mir-503, hsa-mir-542, hsa-mir-151b, mmu-mir-301b, mmu-mir-146b, mmu-mir-708, hsa-mir-708, hsa-mir-301b, hsa-mir-1246, hsa-mir-1277, hsa-mir-1307, hsa-mir-2115, mmu-mir-486b, mmu-mir-28c, mmu-mir-101c, mmu-mir-28b, hsa-mir-203b, hsa-mir-5680, hsa-mir-5681a, mmu-mir-145b, mmu-mir-21b, mmu-mir-21c, hsa-mir-486-2, mmu-mir-126b, mmu-mir-142b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
One-base-shift forms of miR-9*, miR-148b* and miR-1246 showed higher expression than the reference forms in both metastatic and non-metastatic lines. [score:3]
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Cancer Lett 30 Duursma AM Kedde M Schrier M le Sage C Agami R 2008 miR-148 targets human DNMT3b protein coding region. [score:3]
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[+] score: 2
Other miRNAs from this paper: mmu-mir-148a
MicroRNA-148/152 impair innate response and antigen presentation of TLR-triggered dendritic cells by targeting CaMKIIα. [score:2]
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Serum miR-152, miR-148a, miR-148b, and miR-21 as novel biomarkers in non-small cell lung cancer screening. [score:1]
MicroRNA-130b PPARγ BCL-2 Apoptosis NSCLC Several microRNAs (miRNAs), such as miR-21, miR-152, miR-148b and miR-208a, play critical roles in lung cancer progression through modulating growth, apoptosis, metastasis and invasion [1– 4]. [score:1]
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Of the 74 metastamiRs identified in this study, we found an overlap of 16 metastamiRs, including Hsa-miR-148b, Hsa-miR-23a, Hsa-miR-100, Hsa-miR-93, Hsa-miR-125b, Hsa-miR-98, Hsa-miR-92a, Hsa-miR-29b, Hsa-miR-30c, Hsa-let-7a, Hsa-let-7b, Hsa-let-7c, Hsa-let-7e, Hsa-let-7f, and Hsa-let-7g, with the findings of other researchers. [score:1]
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It further included miR-146b, miR-210 and multiple members of the miR-148 and miR-181 families. [score:1]
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[+] score: 1
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, 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-200a, 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
Olfactory bulb let-7b, let-7c-1, let-7c-2, miR-10a, miR-16, miR-17, miR-21, miR-22, miR-28, miR-29c, miR-124a-1, miR-124a-3, miR-128a, miR-135b, miR-143, miR-148b, miR-150, miR-199a, miR-206, miR-217, miR-223, miR-29b-1, miR-329, miR-331, miR-429, miR-451. [score:1]
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86 miR-873-as 1,016 e-miR-743b-5p 23.75 miR-449c-as 515e-miR-715 || 69.35 miR-541-as 439 e-miR-881* 56.21 miR-148b-as 336 e-miR-370 97.41 miR-546-as 333 e-miR-3067 100 miR-3074-as 262 e-miR-448-5p 100miR-451-as ‡ 286 e-miR-669o-5p 99.35 † Novel miR* that are processed within the expected window of the mature strand are labelled “generic”. [score:1]
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Other miRNAs from this paper: hsa-let-7a-2, hsa-let-7c, hsa-let-7e, hsa-mir-15a, hsa-mir-16-1, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-2, hsa-mir-100, hsa-mir-29b-2, mmu-let-7i, mmu-mir-99b, mmu-mir-125a, mmu-mir-130a, mmu-mir-142a, mmu-mir-144, mmu-mir-155, mmu-mir-183, hsa-mir-196a-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, hsa-mir-148a, mmu-mir-143, hsa-mir-181c, hsa-mir-183, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-298, mmu-mir-34b, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-130a, hsa-mir-142, hsa-mir-143, hsa-mir-144, hsa-mir-125a, mmu-mir-148a, mmu-mir-196a-1, mmu-let-7a-2, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-mir-15a, mmu-mir-16-1, mmu-mir-21a, mmu-mir-22, mmu-mir-23a, mmu-mir-24-2, rno-mir-148b, hsa-mir-200c, hsa-mir-155, mmu-mir-100, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181c, hsa-mir-34b, hsa-mir-99b, hsa-mir-374a, hsa-mir-148b, rno-let-7a-2, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7i, rno-mir-21, rno-mir-22, rno-mir-23a, rno-mir-24-2, rno-mir-29b-2, rno-mir-34b, rno-mir-99b, rno-mir-100, rno-mir-124-1, rno-mir-124-2, rno-mir-125a, rno-mir-130a, rno-mir-142, rno-mir-143, rno-mir-144, rno-mir-181c, rno-mir-183, rno-mir-199a, rno-mir-200c, rno-mir-200b, rno-mir-181a-1, rno-mir-298, hsa-mir-193b, hsa-mir-497, hsa-mir-568, hsa-mir-572, hsa-mir-596, hsa-mir-612, rno-mir-664-1, rno-mir-664-2, rno-mir-497, mmu-mir-374b, mmu-mir-497a, mmu-mir-193b, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-568, hsa-mir-298, hsa-mir-374b, rno-mir-466b-1, rno-mir-466b-2, hsa-mir-664a, mmu-mir-664, rno-mir-568, hsa-mir-664b, mmu-mir-21b, mmu-mir-21c, rno-mir-155, mmu-mir-142b, mmu-mir-497b, rno-mir-148a, rno-mir-15a, rno-mir-193b
The terminal 5' exon of orthologous transcript NP_001101587.1 in rat is missing, locating miR-148b upstream of NP_001101587.1; (c) Rat miR-142 is located in the first exon of the alternatively spliced transcript Q9JIR0-2. The orthologous alternative transcripts in human and mouse lacks the 5' exon, placing human and mouse miR-142 upstream of the BZRAP1 transcript. [score:1]
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In the serum, IPA indicates that miR-125b alters p53, IL-12, and TNF; miR-29c alters IL-12 and IL-6; miR-15a alters VEGF and IL-6; and miR-148b alters PTEN (Fig 9). [score:1]
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Several other studies have studied the role of miR-21, miR-34, miR-9, miR-132, miR-140, miR-148b-3p, miR-210, miR-29a, miR-709 in SC proliferation and migration in vitro 8, 17, 26, 28, 39– 43. [score:1]
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