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34 publications mentioning mmu-mir-151

Open access articles that are associated with the species Mus musculus and mention the gene name mir-151. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 114
In addition, the co -expression of two pairs of miRNAs also led to a significantly increased repression: miR-151 + miR-337 resulted in a synergistic inhibition of 78% and miR-145a + miR-151 repressed TWIST1 expression by 61% (p<0.006). [score:7]
Inhibition of miR-145a-5p, miR-151-5p and miR-337-3p resulted in a decreased repression, i. e. an elevated expression of the reporter protein in both cell lines (Fig. 6C and 6D), confirming that the endogenous murine miRNAs are able to target the Twist1 3′UTR. [score:7]
However, miR-151 has been shown to be both upregulated (HCC, nasopharyngeal carcinoma) and downregulated (pappillary carcinoma, acute myeloid leukemia) in different types of cancer [46]. [score:7]
MiRNA target site/Species Human Mouse Cow Dog Chicken FrogTargeting Twist2 miR-15b-3p + − + + − − − miR-33-5p + + + + − + − miR-137-3p + + + + − + − miR-145a-5p + + + + − − + miR-151-5p + + + + − + − miR-214-5p + + + + − − − miR-326-3p + + + + − − − miR-337-3p + + + + − + − miR-361-5p + + + + − − − miR-378a-5p + + + + − − − miR-381-3p + + + + − + − miR-409-3p + + + + − − − miR-450b-5p + + + + − + − miR-508-3p + + + + − − − miR-543-3p + + + + − − − miR-576-5p + + + + − − − miR-580 + + + + − − − miR-591 + + + + − − − MicroRNAs underlined were tested in this study. [score:5]
In fact, we assume that the relatively high expression of endogenous miR-151-5p in H1299 cells (publically available miRNA microarray dataset; GEO accession number GSE30075) explains the significant difference between the miR-151-5p -mediated repressive effects shown in figures 2 and 3. The distance between miR-145a-5p and miR-151-5p target sites is 394 nt, too long to expect a synergistic interaction [34]. [score:5]
This indicates that the synergistic effect of miR-151-5p and miR-337-3p is mainly due to translational inhibition and not RNA degradation. [score:5]
In light of our results, it would be interesting to see whether miR-337 is able to acquire a tumor suppressor function when co-expressed with miR-151 in TWIST1 positive tumors. [score:5]
As shown in Fig. 6A and 6B, endogenous miR-145a-5p, miR-151-5p and miR-337-3p are targeting Twist1 3′UTR in both cell lines, as mutating their target sites led to a statistically significant increase of reporter activities. [score:5]
MiR-151 targets the thrombopoietin receptor MPL [43], a gene known to be downregulated in myeloproliferative neoplasms [44]. [score:5]
In contrast, the combinatorial effect of miR-151-5p and miR-337-3p clearly is synergistic, as miR-337-3p alone was not able to downregulate the Twist1 3′UTR reporter but only did so when miR-151-5p was present (Fig. 3). [score:4]
We analyzed the presence of conserved miRNA target sites in the 3′UTR of Twist1 in selected amniotes (Table 1 and 2) and identified miR-145a-5p, miR-151-5p and the combinations of miR-145a-5p + miR-151-5p and miR-151-5p + miR-337-3p as the strongest regulators of murine Twist1 (Fig. 2 and 3). [score:4]
As the uneven ratio between Twist1 mRNA and TWIST1 protein in the mouse embryo [23], [24] indicated translational inhibition, we compared the mRNA and protein ratios in cells treated with a combination of synthetic miR-151-5p and miR-337-3p precursors. [score:4]
50 nM miRCURY LNA microRNA inhibitors (Exiqon) were added in the inhibition assay: mmu-miR-145a-5p (139465-00), hsa-miR-151-5p (414654-00), mmu-miR-337-3p (139530-00) and a Scrambled negative control (199004-00). [score:4]
MiRNA target sites were subsequently mutated to restriction enzyme recognition sites: miR-145a-5p to SacI; miR-151-5p to AgeI; miR-337-3p to SalI. [score:3]
It would thus be interesting to investigate whether the expression of miR-151 in tumors correlates with the expression level of TWIST1. [score:3]
So far, nothing is known about the co -expression of miR-151 and miR-337. [score:3]
Interestingly, the target sites for miR-151-5p and miR-337-3p will still be present, even if the previously reported shortening of 3′UTRs in cancer cells [35] also occurs with TWIST1 and either the first or the second pA signal should be used. [score:3]
As shown in Fig. 3, mutating the target site of miR-145a-5p or miR-151-5p resulted in a loss of repression whereas lack of a binding site for miR-337-3p had no effect. [score:3]
Since miR-145a-5p, miR-151-5p and miR-337-3p all were expressed in NIH-3T3 and C3H/10T1/2 but not in C [2]C [12] cells, we selected the first two lines for further analysis. [score:3]
Importantly, this synergistic effect was not observed if the miR-151-5p target site was mutated. [score:3]
Interestingly, miR-337 was only able to repress the 3′UTR reporter when miR-151 and its target site both were present. [score:3]
When both miR-145a and miR-151 were present, mutating either of the target sites caused a comparable loss of repression. [score:3]
The following miRNAs were tested for their potential to repress Twist1 translation in the human lung carcinoma cell line H1299: miR-33, miR-145a, miR-151, miR-326, miR-337, miR-361, miR-378a, miR-381, miR-409 and miR-543 (Fig. 1). [score:3]
The probabilities of cell migration were estimated as 0.898 (95% bootstrap CI 0.896–0.913) for the miR-151-5p + miR-337-3p treated cells and 0.918 (95% bootstrap CI 0.914–0.922) for the control treated cells, and a bootstrap permutation test (p-value 0.000135) showed that the difference between the probabilities is statistically significant. [score:2]
In summary, we have shown that TWIST1 is regulated by miR-145a-5p, miR-151-5p and miR-337-3p. [score:2]
However, the high statistical significance of the difference indicates that the treatment with miR-151-5p and miR-337-3p has a reliable effect. [score:1]
While seeding, cells were transiently transfected with a total of 20 nM pre-mmu-miR-151-5p (PM11537) and pre-mmu-miR-337-3p (PM12817) or with Scrambled Negative Control #1 (AM17110; all Applied Biosystems) using Lipofectamine 2000 (Invitrogen) according to manufacturer's instructions. [score:1]
Dot-plot superposed with the box-plot of the predicted probabilities of cell migration for observations from miR-151-5p + miR-337-3p (red) and scrambled control (blue) treated cells (p-value 0.000135). [score:1]
To more closely mimic the physiological conditions, we established stable pools of cells harboring the Twist1 3′UTR reporter and transfected them using low concentrations (5 nM) of synthetic miR-151-5p and miR-337-3p precursors. [score:1]
In hepatocellular carcinoma (HCC), miR-151-5p has been correlated with cell migration and intrahepatic metastasis [45]. [score:1]
In addition, miR-337-3p has no complementary sequence to Twist1 5′ of its seed region leaving this sequence free for miR-151-5p to bind. [score:1]
The miRBase accession numbers for miRNAs are: mmu-miR-33 (MI0000707), mmu-miR-145a (MI0000169), mmu-miR-151 (MI0000173), mmu-miR-326 (MI0000598), mmu-miR-337 (MI0000615), mmu-miR-361 (MI0000761), mmu-miR-378a (MI0000795), mmu-miR-381 (MI0000798), mmu-miR-409 (MI0001160) and mmu-miR-543 (MI0003519). [score:1]
Using high concentrations of pre-miR-151-5p and pre-miR-337-3p (above 10 nM) we consistently found comparable decrease in both the mRNA and protein level of the Twist1 3′UTR reporter (Fig. 4A). [score:1]
0066070.g007 Figure 7Dot-plot superposed with the box-plot of the predicted probabilities of cell migration for observations from miR-151-5p + miR-337-3p (red) and scrambled control (blue) treated cells (p-value 0.000135). [score:1]
Note the presence of miR-151-5p + miR-337-3p treated cells with extreme low estimates of probability of cell migration. [score:1]
MiR-337 always required miR-151 to be present in order to have an effect. [score:1]
MiR-151-5p and miR-337-3p reduce the mobility of murine embryonic fibroblast cells. [score:1]
The reduced mobility of miR-151-5p + miR-337-3p treated embryonic fibroblasts further shows the therapeutic potential in the combination of these two miRNAs (Fig. 7). [score:1]
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[+] score: 94
In this study, the expression of miR-151-5p was found to be upregulated at all time points assessed, in contrast to reports that its expression was downregulated in response to infection with H1N1 and H5N1 [25, 61]. [score:11]
Groups of mice (n = 25) were transfected with 30 ug of miRNA inhibitors (miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p) or an miRNA negative inhibitor control (miRNA negative inhibitor control #1; Bioneer Co. [score:7]
Groups of 8 (done twice, total 16) or 9 (lung viral titration) C57BL/6 mice were inoculated intranasally with ma81 H5N2 avian influenza virus (5 MLD50) 24 hours after individual transfection of 30 μg miRNA inhibitors (miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p) or an miRNA negative inhibitor control (miRNA negative inhibitor control #1; Bioneer Co. [score:7]
It is important to note that only 9 miRNAs (miR-100-5p, miR-130a-5p, miR-146b-3p, miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p, miR-301a-3p, and miR-495-3p) were significantly upregulated or downregulated in both lungs infected with either wild type w81 or the mouse-adapted ma81 strain at all time points (Tables  1 and 2). [score:7]
Furthermore, inhibition of miR-151-5p expression reduced influenza virus titers compared to those of infected lungs from mice not treated with the inhibitor, and 30% of mice treated with anti-miR-151-5p regained their body weight and survived influenza infection (Figure  6). [score:6]
Twenty-seven and 20 differentially expressed miRNAs identified to be commonly presented at 1 and 3 dpi were presented in Tables  3 and 4. Of these, only miR-100-5p, miR-130a-5p, miR-146b-3p, miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p, miR-301a-3p, and miR-495-3p were commonly upregulated at both 1 and 3 dpi. [score:6]
In our study, the expression of miR-151-5p in lungs infected with the influenza virus was found to be upregulated at all time points examined. [score:6]
Although the specific miRNA inhibitors could not completely attenuate mortality or reduce viral replication, the miR-151-5p- and miR-223-3p -inhibitors reduced mortality of inoculated mice to 70% and substantially delayed death. [score:5]
Thus, these results indicate that inhibition of miR-151-5p and miR-223-3p reduces influenza replication in the lungs, while the overexpression of these miRNAs in the lungs augments influenza infection. [score:5]
Among the 238 differentially expressed miRNAs, we selected 4 miRNAs with greater than 2-fold differences in expression levels in the lungs of mice that were infected with either w81 or ma81 compared to mock control infections for in-depth analyses (miRNAs are miR-151-5p, miR-223-3p, miR-147-3p, and miR-155-3p) (Table  5). [score:4]
It is noteworthy that only 9 miRNAs (miR-100-5p, miR-130a-5p, miR-146b-3p, miR-147-3p, miR-151-5p, miR-155-3p, miR-223-3p, miR-301a-3p, and miR-495-3p) were significantly upregulated in both lungs infected with either wild type w81 or the mouse-adapted ma81 strain at both time points. [score:4]
Altogether, we can speculate that the silencing of miR-151-5p expression alters the pathogenesis of the influenza virus and promotes the antiviral ability of the host during influenza infection. [score:3]
Inhibition of miR-147-3p, miR-151-5p, miR-155-3p, and miR-223-3p confers viral pathogenesis in mice. [score:3]
Notably, expression levels of miR-151-5p, miR-223-3p, miR-147-3p, and miR-155-3p were higher in the lungs of mice infected with the ma81 virus than those infected with the w81 virus. [score:3]
Ding et al. highlighted the detrimental role of overexpressed miR-151-5p in the pathogenesis of hepatocellular carcinoma (HCC). [score:3]
Notably, expression levels of miR-147-3p, miR-151-5p, miR-155-3p, and miR-223-3p were higher in the lungs of mice infected with the ma81 virus than those infected with the w81 virus. [score:3]
In their study, significantly increased HCC cell migration and invasion were observed when miR-151-5p, together with its host gene (encoding focal adhesion kinase), was overexpressed. [score:3]
Potential roles of miR-151-5p may be related to the previously identified function of this molecule in the regulation of tumor cell migration and spreading of hepatocellular carcinoma [60]. [score:2]
There were 3, 4, and 4 immune- and cell death-related GO terms of molecular function were enriched for the miR-151-5p, miR-155-3p, and miR-223-3p, respectively. [score:1]
Moreover, the mice treated with anti-miR-151-5p and anti-miR-223-3p began to gain weight starting at 6 dpi and rapidly recovered their body weight thereafter (Figure  6). [score:1]
Approximately 37.5% (6 out of 16) and 25% (4 out of 16) of mice treated with anti-miR-151-5p and anti-miR-223-3p, respectively, survived until the end of the experiment, whereas all untreated control mice were dead by 7 dpi. [score:1]
These miRNAs include miR-151-5p, miR-223-3p, miR-147-3p, and miR-155-3p (Table  5). [score:1]
Specifically, these miRNAs have been implicated in immune responses (miR-223-3p and miR-147-3p), viral infection (miR-155-3p), and cell migration (miR-151-5p) [50- 56]. [score:1]
A: miR-147-3p, B: miR-151-5p, C: miR-155-3p, D: miR-233-3p. [score:1]
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[+] score: 55
gov/pubmed, as of 5/3/2012) Name Relationship: liver Relationship: bile ductmiR-126-3pNo reportNo reportmiR-30bInhibited TGF beta1 -induced EMT, [24] downregulated after hepatectomy in rats [29]Upregulated in LPS -induced Activated NFκB in cholangiocytes [25]miR-30cRequired for hepatobiliary development [10]Required for hepatobiliary development, [10] upregulated after C. parvum infection [26]miR-151-3pNo reportNo reportmiR-320Downregulated in Huh7 cells after HCV infection [21]Downregulated in intrahepatic cholangiocarcinoma, involved in drug-triggered apoptosis [28]miR-676No reportNo reportmiR-204No reportDownregulated in intrahepatic cholangiocarcinoma [28]miR-193bDownregulated in HCC, [13] upregulated in a HCC cell line after transfection of HCV genome [20]No reportmiR-365No reportNo reportmiR-133aNo reportNo reportmiR-200bDownregulated in HCC, [18, 19] upregulated in NAFLD and NASH [22, 23]Upregulated in cholangiocarcinoma cell lines [27]miR-133bNo reportNo reportmiR-200aDownregulated in HCC [15] and inhibited the proliferation and migration of HCC cells, [17] upregulated in NAFLD [23]No report miR-195Downregulated in HCC, [15] suppressed growth of HCC, [14] sensitized HCC to 5-fluorouracil, [16] inhibited proliferation of HSC [30] No report TGF: transforming growth factor, LPS: lipopolysaccharide, HCC: hepatocellular carcinoma, HCV: Hepatitis C virus, EMT: epithelial-to-mesenchymal transition, NAFLD: nonalcoholic fatty liver disease, NASH: nonalcoholic steatohepatitis, HSC: hepatic stellate cells. [score:55]
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[+] score: 32
Putative targets of nine differentially expressed miRNAs that were validated by RT-qPCR (upregulated: mmu-miR-151-3p, mmu-miR-155-5p, mmu-miR-181a-5p, and mmu-miR-328-3p; and downregulated: mmu-miR-21a-5p, mmu-miR-98-5p, mmu-miR-145a-5p, mmu-miR-146b-5p, and mmu-miR-374b-5p) were obtained from the miRWalk database. [score:11]
According to the expression levels and fold-change comparing Brucella-infected versus NI libraries, we selected four miRNAs that were upregulated (mmu-miR-151-3p, mmu-miR-155-5p, mmu-miR-181a-5p, and mmu-miR-328-3p) and five miRNAs that were downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, mmu-miR-145a-5p, mmu-miR-146b-5p, and mmu-miR-374b-5p) for validation and further analysis. [score:9]
For further validation, we chose four upregulated (mmu-miR-151-3p, mmu-miR-155-5p, mmu-miR-181a-5p, and mmu-miR-328-3p) and five downregulated (mmu-miR-21a-5p, mmu-miR-98-5p, mmu-miR-145a-5p, mmu-miR-146b-5p, and mmu-miR-374b-5p) miRNAs (Table S6 in) in infected samples by real-time PCR in macrophages. [score:7]
Four miRNAs were validated by real-time PCR as upregulated: (A) mmu-miR-151-3p, (B) mmu-miR-155-5p, (C) mmu-miR-181a-5p, and (D) mmu-miR-328-3p. [score:4]
C57BL/6 mice were infected intraperitoneally at 1, 3, or 6 days post-infection, and the relative expression of miRNAs: (A) mmu-miR-151-3p, (B) mmu-miR-155-5p, (C) mmu-miR-181a-5p, (D) mmu-miR-328-3p, (E) mmu-miR-21a-5p, (F) mmu-miR-98-5p, (G) mmu-miR-145a-3p, (H) mmu-miR-146b-5p, and (I) mmu-miR-374b-5p were evaluated in mouse spleens. [score:1]
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[+] score: 18
Selection of the differentially expressed miRNAs under the relatively strict conditions (≥500 sequence reads in at least one of the libraries selected for comparison, ≥5-fold difference in expression, and a p value of ≤ 0.01) identified nine upregulated miRNAs (let-7e-5p, miR-101a-3p, miR-151-5p, miR-181a-5p, miR-204-5p, miR-340-5p, miR-381-3p, miR-411-5p, miR-9-5p, and miR-219-2-3p) at 3 d, but none at 7 d or 14 d, suggesting that these upregulated miRNAs impact biological functions, particularly during the early stages after nerve allotransplantation with FK506 immunosuppression. [score:13]
Among the nine upregulated miRNAs (let-7e-5p, miR-101a-3p, miR-151-5p, miR-181a-5p, miR-204-5p, miR-340-5p, miR-381-3p, miR-411-5p, miR-9-5p, and miR-219-2-3p), miR-9-5p had the highest fold-change (≥50-fold at 3 d), followed by miR-340-5p with 38.8-fold. [score:4]
Nine candidate miRNAs (let-7e-5p, miR-101a-3p, miR-151-5p, miR-181a-5p, miR-204-5p, miR-340-5p, miR-381-3p, miR-411-5p, and miR-9-5p) were identified. [score:1]
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[+] score: 13
There were four up-regulated miRNAs (mmu-miR-709, mmu-miR-467a-3p, mmu-miR-182-5p and mmu-miR-25-5p) and seven down-regulated miRNAs (mmu-miR-615-3p, mmu-miR-409-3p, mmu-miR-680, mmu-miR-129-5p, mmu-miR-151-5p, mmu-miR-142-5p and mmu-miR-30b-5p), as the values presented in Table 1. Then we performed unsupervised hierarchical clustering of the eleven miRNAs. [score:7]
Control) P -valuemmu-miR-25-5p2.210.04mmu-miR-7091.980.02mmu-miR-467a-3p1.820.04mmu-miR-182-5p1.540.05mmu-miR-129-5p0.290.02mmu-miR-6800.340.02mmu-miR-615-3p0.360.00mmu-miR-409-3p0.440.02mmu-miR-30b-5p0.510.05mmu-miR-151-5p0.610.03 mmu-miR-142-5p 0.63 0.04By TargetScan, we found that mmu-miR-25-5p, mmu-miR-615-3p, mmu-miR-151-5p and mmu-miR-680 had few target genes directly relating with Tregs in MeSH database, so we excluded the four miRNAs for further exploration. [score:6]
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[+] score: 13
We also explored the effects on the signalling pathways of the first nine highly expressed miRNAs and discovered that miR-666-3p, miR-540-3p, miR-125b-5p and miR-450b-3p potentially promote FoxO1 expression, whereas miR-883b-5p, 666-3p, miR-450b-3p and miR-151-3p may play an essential role in down-regulation of Glut4 expression. [score:10]
It is worth mentioning that one of the predicted genes of miR-151-3p is Ppp2r5b (protein phosphatase 2, regulatory subunit B’, beta isoform) (Supplementary Information datasheet  6), which has been linked to insulin resistance in adipocytes [35]. [score:2]
According to the microRNA microarray analysis, the first nine highly expressed miRNAs (miR-883b-5p, miR-666-3p, miR-770-5p, miR-804, miR-540-3p, miR-882, miR-125b-5p, miR-450b-3p, and miR-151-3p) were selected out for further investigation. [score:1]
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[+] score: 11
In the ileum, IPA indicated that increases in miR-34a-5p alters NF-κB; let-7g and miR-98 regulates STAT3; miR-34a, mR-188-5p, let-7a-5p, and miR-151-5p regulate MAPK; miR-20b regulates IL-10; let-7g and miR-98 regulate IL-10, IL-13, IL-6; miR-15b regulates IL-6; whereas miR-99a and miR-100 regulate TNF (Fig 8). [score:7]
Also, the former was predicted to be indirectly targeted by increases in miR-188-5p, let-7, and miR-151-5p. [score:4]
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[+] score: 10
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-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-148b, 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
Furthermore, some of the differentially expressed miRNAs have been reported to play a role in the metastasis of other types of cancer, for example, the up-regulated miRNAs, let-7i, miR-9, miR-30a, miR-125b, miR-142-5p, miR-151-3p, miR-450a and the down-regulated miRNAs, miR-24, mir-145, miR-146b-5p, miR-185, miR-186, miR-203 and miR-335. [score:9]
The miR-30a, miR-142-5p and miR-450a have roles in metastatic breast and colon cancer [61] and the miR-151-3p can enhance hepatocellular carcinoma cell mobility [66]. [score:1]
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[+] score: 9
Our previous studies showed that genistein treatment significantly down-regulated the expression of oncogenic miR-151 which directly targets SOX17 and ARHGDIA [17]. [score:9]
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[+] score: 9
Figure 2B displays discrepancies between the miRNA array and RT-qPCR data, showing that only 3 down-regulated miRNAs (miR-150, miR-28 and miR-151-5p) and 8 upregulated miRNAs (miR-let-7e, miR-103, miR-107, miR-27a, miR-23a, miR-21, miR-155 and miR-146a) showed similar trends in altered miRNA levels. [score:7]
miR-28, miR-150, and miR-151-5p levels in CD4+PD1+ T cells decreased by 30%, 45%, and 25%, respectively (Figure 2C). [score:1]
Based on our microarray and qPCR results, three miRNA (miR-28, miR-150, miR-151-5p) were confirmed decreased in CD4+PD1+ T cells. [score:1]
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[+] score: 9
We found that miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107 were differentially expressed in a BLM -induced mouse mo del of pulmonary fibrosis (Fig. 1C). [score:3]
miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107 were differentially expressed in mouse fibrotic lung tissues. [score:3]
Five miRNAs, miR-21, miR-455, miR-151-3p, miR-486-5p and miR-3107, were validated to be dysregulated in the lung tissues from mice with silica -induced fibrosis (n = 6 per group) (Fig. 1B). [score:2]
The expression of mature miRNAs was assayed using TaqMan MicroRNA Assays (Applied Biosystems, Foster City, CA) specific for hsa-miR-486 (ID 001278), hsa/mmu-miR-21a (ID 000397), hsa-miR-455 (ID 001280), hsa-miR-151-3p (ID 002254), mmu-miR-1a (ID 002222), mmu-miR-133b (ID 002247), mmu-miR-5128 (ID 462199_mat), mmu-miR-223 (ID 002295), mmu-miR-146b (ID 001097), mmu-miR-133a (ID 001637), mmu-miR-449a (ID 001030), mmu-miR-122 (ID 002245), mmu-miR-351-3p (ID 464446_mat), mmu-miR-193a-5p (ID 002577), mmu-miR-151-3p (ID 001190), mmu-miR-574-3p (ID 002349), mmu-miR-3107/486 (ID 001278). [score:1]
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[+] score: 6
Target sites in the 5′UTR and coding region, which were both in silico predicted and the corresponding miRNAs enriched in Rac1-miR-CATCH comprised let-7a/e-5p, miR-9-5p, miR-26a-5p, miR-151-3p and miR-652-3p (Fig. 4d and Table 3a). [score:3]
In addition, a number of candidate miRNAs, which were both predicted to target Rac1 and were enriched in Rac1-miR-CATCH were found, e. g. miR-103-3p, let-7a/c/e/f-5p, miR-320-3p, miR-9-5p, miR-26a-5p, miR-151-3p (Fig. 4d and Table 3a). [score:3]
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Interestingly, the certain miRNAs, such as miR-96, miR-140, miR-151, miR-185, miR-378, miR-455, miR-532, and miR-874, presumably targeting a 3’UTR of INSR, were upregulated by more than 1.5-fold in the liver of HFD mice compared to NFD-fed control, whereas the levels of other selected miRNAs remained unaffected (S2 Fig). [score:5]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-21, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-9-2, mmu-mir-10b, hsa-mir-192, mmu-mir-194-1, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-122, hsa-mir-10a, hsa-mir-10b, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-210, hsa-mir-214, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-122, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-194-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-21a, mmu-mir-10a, mmu-mir-210, mmu-mir-214, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-9-1, mmu-mir-9-3, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-365a, mmu-mir-365-1, hsa-mir-365b, hsa-mir-151a, gga-let-7i, gga-let-7a-3, gga-let-7b, gga-let-7c, gga-mir-16-1, gga-mir-194, gga-mir-10b, gga-mir-199-2, gga-mir-16-2, gga-let-7g, gga-let-7d, gga-let-7f, gga-let-7a-1, gga-mir-199-1, gga-let-7a-2, gga-let-7j, gga-let-7k, gga-mir-122-1, gga-mir-122-2, gga-mir-9-2, mmu-mir-365-2, gga-mir-9-1, gga-mir-365-1, gga-mir-365-2, hsa-mir-151b, mmu-mir-744, gga-mir-21, hsa-mir-744, gga-mir-199b, gga-mir-122b, gga-mir-10a, gga-mir-16c, gga-mir-214, sma-let-7, sma-mir-71a, sma-bantam, sma-mir-10, sma-mir-2a, sma-mir-3479, sma-mir-71b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, gga-mir-365b, sma-mir-8437, sma-mir-2162, gga-mir-9-3, gga-mir-210a, gga-mir-9-4, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3, gga-mir-9b-1, gga-mir-10c, gga-mir-210b, gga-let-7l-1, gga-let-7l-2, gga-mir-122b-1, gga-mir-9b-2, gga-mir-122b-2
Of the 10 miRNAs examined, all except miR-365 and miR-151 were differentially expressed between naïve and infected mice by 6–8 weeks post infection (Fig. 1, Table S2). [score:3]
Consistent with the array results, there was an increase in miR-199-5p, miR-199-3p, miR-214, miR-21, miR-210, and a reduction of miR-192, miR-194, miR-365, miR-122 and miR-151 in the liver tissue of S. mansoni infected mice as compared to naïve mice; miR-9 and miR-744 did not display differential expression and were not analysed further (Table 1). [score:2]
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In addition to well-known myomiRs, recent studies have demonstrated that miR-486 [49], miR-378 [50], miR181a [80], miR-21a, miR-101a, and miR-151 [54] are also involved in regulation of myogenesis and several other ubiquitously expressed miRNAs have also been found to participate in myogenesis, including miR-26a [51], miR-27b [52, 53], and miR-29 [44]. [score:4]
Of the 8 known miRNAs examined, 7 miRNAs (miR-425, miR-26a, miR-1a, miR-199a, miR-101, miR-378, and miR-151) showed a consistent pattern with the deep sequencing data (Figures 6(a)– 6(j)). [score:1]
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Three microRNAs had decreased expression in the bleomycin treated lungs (miR-26a, miR-151-3p and miR-676) while eight microRNAs had increased expression in the bleomycin treated lungs (miR-146b, miR-199a-5p, miR-21, miR-34a, miR-335-5p, miR-207, miR-301a and miR-449a). [score:5]
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While the knowledge of how, in turn, miRNA expression is controlled in cancer remains limited, many HCC-related miRNAs have been shown to be silenced as a result of CpG hypermethylation, whereas others, such as miR-151, are overexpressed in HCC because of a chromosomal region gain (8q24 in case of miR-151) [53]. [score:5]
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Other miRNAs from this paper: hsa-mir-25, hsa-mir-28, hsa-mir-95, mmu-mir-290a, mmu-mir-297a-1, mmu-mir-297a-2, mmu-mir-130b, mmu-mir-340, mmu-mir-25, mmu-mir-28a, hsa-mir-130b, hsa-mir-367, hsa-mir-372, hsa-mir-378a, mmu-mir-378a, hsa-mir-340, hsa-mir-151a, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-505, hsa-mir-506, mmu-mir-367, hsa-mir-92b, hsa-mir-548a-1, hsa-mir-548b, hsa-mir-548a-2, hsa-mir-548a-3, hsa-mir-548c, hsa-mir-648, hsa-mir-548d-1, hsa-mir-548d-2, hsa-mir-659, hsa-mir-421, hsa-mir-151b, hsa-mir-1271, hsa-mir-378d-2, mmu-mir-467b, mmu-mir-297b, mmu-mir-505, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, mmu-mir-421, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, mmu-mir-466c-1, mmu-mir-466e, mmu-mir-466f-1, mmu-mir-466f-2, mmu-mir-466f-3, mmu-mir-466g, mmu-mir-466h, mmu-mir-467c, mmu-mir-467d, mmu-mir-92b, mmu-mir-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-669g, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, mmu-mir-1195, hsa-mir-548e, hsa-mir-548j, hsa-mir-1285-1, hsa-mir-1285-2, hsa-mir-1289-1, hsa-mir-1289-2, hsa-mir-548k, hsa-mir-1299, hsa-mir-548l, hsa-mir-1302-1, hsa-mir-1302-2, hsa-mir-1302-3, hsa-mir-1302-4, hsa-mir-1302-5, hsa-mir-1302-6, hsa-mir-1302-7, hsa-mir-1302-8, hsa-mir-548f-1, hsa-mir-548f-2, hsa-mir-548f-3, hsa-mir-548f-4, hsa-mir-548f-5, hsa-mir-1255a, hsa-mir-548g, hsa-mir-548n, hsa-mir-548m, hsa-mir-548o, hsa-mir-1268a, hsa-mir-548h-1, hsa-mir-548h-2, hsa-mir-548h-3, hsa-mir-548h-4, hsa-mir-548p, hsa-mir-548i-1, hsa-mir-548i-2, hsa-mir-548i-3, hsa-mir-548i-4, hsa-mir-1255b-1, hsa-mir-1255b-2, mmu-mir-1906-1, hsa-mir-1972-1, hsa-mir-548q, mmu-mir-466m, mmu-mir-466o, mmu-mir-467a-2, mmu-mir-467a-3, mmu-mir-466c-2, mmu-mir-467a-4, mmu-mir-466b-4, mmu-mir-467a-5, mmu-mir-466b-5, mmu-mir-467a-6, mmu-mir-466b-6, mmu-mir-467a-7, mmu-mir-466b-7, mmu-mir-467a-8, mmu-mir-467a-9, mmu-mir-467a-10, mmu-mir-466p, mmu-mir-466n, mmu-mir-466b-8, hsa-mir-3116-1, hsa-mir-3116-2, hsa-mir-3118-1, hsa-mir-3118-2, hsa-mir-3118-3, hsa-mir-548s, hsa-mir-378b, hsa-mir-466, hsa-mir-548t, hsa-mir-548u, hsa-mir-548v, hsa-mir-3156-1, hsa-mir-3118-4, hsa-mir-3174, hsa-mir-3179-1, hsa-mir-3179-2, hsa-mir-3179-3, hsa-mir-548w, hsa-mir-3156-2, hsa-mir-3156-3, hsa-mir-548x, mmu-mir-3470a, mmu-mir-3470b, mmu-mir-3471-1, mmu-mir-3471-2, hsa-mir-378c, hsa-mir-1972-2, hsa-mir-1302-9, hsa-mir-1302-10, hsa-mir-1302-11, mmu-mir-1906-2, hsa-mir-3683, hsa-mir-3690-1, hsa-mir-548y, hsa-mir-548z, hsa-mir-548aa-1, hsa-mir-548aa-2, hsa-mir-548o-2, hsa-mir-1268b, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-548h-5, hsa-mir-548ab, hsa-mir-378f, hsa-mir-378g, hsa-mir-548ac, hsa-mir-548ad, hsa-mir-548ae-1, hsa-mir-548ae-2, hsa-mir-548ag-1, hsa-mir-548ag-2, hsa-mir-548ah, hsa-mir-378h, hsa-mir-548ai, hsa-mir-548aj-1, hsa-mir-548aj-2, hsa-mir-548x-2, hsa-mir-548ak, hsa-mir-548al, hsa-mir-378i, hsa-mir-548am, hsa-mir-548an, mmu-mir-28c, mmu-mir-378b, mmu-mir-28b, hsa-mir-548ao, hsa-mir-548ap, mmu-mir-466q, hsa-mir-548aq, hsa-mir-548ar, hsa-mir-548as, hsa-mir-548at, hsa-mir-548au, hsa-mir-548av, hsa-mir-548aw, hsa-mir-548ax, hsa-mir-378j, mmu-mir-378c, mmu-mir-378d, hsa-mir-548ay, hsa-mir-548az, hsa-mir-3690-2, mmu-mir-290b, hsa-mir-548ba, hsa-mir-548bb, hsa-mir-3179-4, mmu-mir-466c-3, hsa-mir-548bc, mmu-mir-1271
In Figure 8E, how miR-151 exerts this function by targeting RhoGDIA to activate Rac1, Cdc42 and Rho GTPases is shown [76]. [score:3]
The functional networks of miR-92b (PRdmiR, mir-25 family, derived from GC rich tandem repeats), miR-28 (RdmiR, mir-28 family, derived from LINE), miR-151 (RdmiR, mir-28 family, derived from LINE), miR-421 (RdmiR, mir-95 family, derived from LINE), miR-1271 (RdmiR, mir-1271 family, derived from LINE), miR-340 (RdmiR, mir-340 family, derived from DNA transportable element) and miR-378 (RdmiR, mir-378 family, derived from SINE) have been reconstructed (Figure 8). [score:1]
In addition, miR-151 can function synergistically with its host gene FAK to enhance HCC cell motility and spreading [76]. [score:1]
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Other miRNAs from this paper: mmu-mir-142a, mmu-mir-195a, mmu-mir-100, mmu-mir-195b, mmu-mir-142b
Study from He's group reveals that chromosome gain of miR-151 augments metastasis of HCC cells by directly targeting RhoGDIA, and consequently activates Rac1 [30]. [score:4]
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The most abundant miRNA species in the liver 20, miR-122-5p, was the highest increased circulating miRNA but other species were elevated to comparable degrees (miR-885-5p, miR-151-3p) or were ranked higher by random forest analysis in terms of ability to report injury (miR-382-5p). [score:1]
miR-122-5p, miR-885-5p, miR-151-3p and miR-382-5p reported acute liver injury due to causes other than acetaminophen, which is consistent with them being liver specific and demonstrates that this panel has utility in the diagnosis of acute liver injury due to multiple causes. [score:1]
The largest fold change miRNAs (miR-122-5p, miR-885-5p and miR-151-3p) and the best discriminating miRNA (miR-382-5p) were taken forward and tested for specificity. [score:1]
Comparative biomarker profiles for miR-122-5p, miR-885-5p, miR-151-3p and miR-382-5p are summarized in supplementary Table 5. Although miR-122-5p had the highest fold increase in APAP-TOX patients, it was ranked 11th place in the miRNA panel, suggesting that other microRNA species may have greater clinical utility. [score:1]
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miRNAs that were differentially expressed only in the LW during aging include miR-29c, miR-705, miR-99a, miR-127, miR-130a, miR-145, miR-151-5p, miR-379, miR-467a, and miR-574-3p. [score:3]
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Other miRNAs from this paper: mmu-mir-182, mmu-mir-19b-2, mmu-mir-19a, mmu-mir-19b-1, mmu-mir-494
In the latest studies, for example, miR-182, miR-151-3p, miR-320a and miR-494 have been reported to exert their essential roles in modulating the metastasis of breast cancer cells through targeting SNAI1, TWIST1, MTDH, PAK1 and so on [6– 9]. [score:3]
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For example, hsa-miR-145, miR-151-3p and miR-30 families align with their mmu-miR counterparts indicating a conserved biological function in breast cancer development in both the genomes (Additional file 1: Figure S1). [score:2]
For example, hsa-miR-145, hsa-miR-151-3p and hsa-miR-30 showed sequence and functional similarity with mmu-miR-145, mmu-miR-151-3p and mmu-miR-30 respectively. [score:1]
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Notable examples of highly expressed miRNAs with unexpected strand bias in HL-1 cells and also in the heart, but having very different strand bias in other tissues [22] are the abundant miR-22*, -322*, -872*, and let-7d*, as well as a marked-5p bias for miR-151-5p. [score:3]
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In contrast, miR-151-3p that regulates full length TrkC-FL mRNA remains unchanged in wild type versus (Fig 4B) and this miRNA serves as internal control. [score:2]
In human SALS there was also a reduction in miR-151-3p (a known disruptor of TrkC-FL) versus non-ALS control and this resulted in a small and non-significant elevation of TrkC-FL mRNA. [score:1]
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Editing levels increased by at least 50% in 11% of all editing events (eight positions in seven miRNAs): miR-376b (position 6), let-7e (positions 17 and 19), miR-381 (position 4), miR-467d* (position 9), miR-3061-3p (position 3), miR-151-3p (position 3), miR-219-3p (position 15). [score:1]
Kawahara Y. Zinshteyn B. Chendrimada T. P. Shiekhattar R. Nishikura K. RNA editing of the microRNA-151 precursor blocks cleavage by the Dicer-TRBP complexEMBO Rep. [score:1]
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Moreover, there is also the first demonstrated elevated levels of miR-874-3p, miR-7a-5p, miR-455-5p, miR-129-1-3p, miR-151-5p, miR-3473b, and down regulated levels of miR-345-3p, novel_mir_8 and let-7 k in the kidneys of db-/db- mice. [score:2]
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Surprisingly, the effects of cigarette smoke on miRNA levels were greater in parenchymal tissues than in tumors (Figure 5 and 7), and miRNA were distributed across three major categories of unequal sizes: 62 mRNA were altered (raw p-values were smaller than 0.05 for the corresponding pairwise comparisons) in parenchyma only, 3 miRNA (mmu-miR-130a-3p, mmu-miR-151-3p, mmu-miR-184-3p) were altered in tumors only and 5 in both tumor and parenchyma. [score:1]
Interestingly, of the 3 miRNA that were affected by cigarette smoke exposure in tumors only, mmu-miR-151-3p, mmu-miR-130a-3p and mmu-miR-184-3p have previously been implicated in carcinogenesis. [score:1]
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At 15 dpi, 17 miRNAs (let-7b,c, miR-10a, miR-21, miR-25, miR-26a, miR-29c, miR-30a,b,c,d, miR-99a, miR-103, miR-151, miR-195, and miR-200b,c) were identified to be important in the late repair phase. [score:1]
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Other miRNAs from this paper: mmu-mir-132, mmu-mir-21a, mmu-mir-433, mmu-mir-21b, mmu-mir-21c
RNA editing of the microRNA-151 precursor blocks cleavage by the Dicer–TRBP complex. [score:1]
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These changes are specific as other miRNAs, including miR-10a, miR-30b, miR-200b and miR-151, are not changed in amount regardless of the origin, whether from the exosomes of cultured tumour cells or metastatic CT26 cells, suggesting that the microenvironment has an effect on the composition of the exosomal miRNA profile. [score:1]
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These are mir-17, mir-22, mir-28, mir-32, mir-128b, mir-135b, mir-143, mir-151, mir-181b-2, mir-205, mir-213, mir-216 and mir-372. [score:1]
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Notch1 pathway -mediated microRNA-151-5p promotes gastric cancer progression [36]. [score:1]
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