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44 publications mentioning mmu-mir-211

Open access articles that are associated with the species Mus musculus and mention the gene name mir-211. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

1
[+] score: 311
Other miRNAs from this paper: hsa-mir-211, hsa-mir-221, mmu-mir-221
We report that miR-211 is downregulated in EOC, inhibits proliferation and induces apoptosis in EOC cells in vitro and that overexpression of miR-211 inhibits growth of EOC xenograft tumors in vivo by repressing Cyclin D1 and CDK6 expression. [score:12]
Relative levels of miRNA expression normalized to U6 snRNA was determined by setting the miRNA expression levels of normal epithelial tissue samples to 1. C. miR-211 expression was downregulated in six EOC cell lines (OVCAR3, Caov3, OVCA429, S KOV3, A2780 and COV644) compared to human ovarian surface epithelial (HOSE) cells. [score:9]
Our results demonstrate that miR-211 is a tumor suppressor that controls expression of Cyclin D1 and CDK6, and that its downregulation results in overexpression of Cyclin D1 and CDK6 which increases proliferation ability of EOC cells to proliferate compared to normal cells. [score:9]
In glioblastoma multiform, miR-211 was found to be downregulated with an inverse correlation of miR-211 expression and matrix metalloproteinase-9 expression [25]. [score:8]
Using mouse embryonic fibroblasts, Chitnis et al. [17] found that miR-211 is a pro-survival molecule that is expressed in a PERK (aka EIF2AK3, Eukaryotic translation initiation factor 2-alpha kinase) -dependent manner and regulates the expression of chop/gadd153 by mediating temporal accumulation of the pro-apoptotic transcription factor chop. [score:8]
In clinical melanoma samples, Mazar et al. [8] found that miR-211 targets KCNMA1, is downregulated in melanoma and that its expression is microphthalma -associated transcription factor dependent. [score:8]
Cyclin D1 and CDK6 were found to be direct targets of miR-211, and when overexpressed in miR-211 -expressing EOC cells, could restore proliferative ability. [score:8]
In summary, we found that miR-211 negatively regulates CDK6 and Cyclin D1 activity and that miR-211 is downregulated in EOC, leading to aberrant expression of CDK6 and Cyclin D1, which results in loss of cell cycle control. [score:7]
Bell et al. found that miR-211 contributes to melanoma adhesion by targeting the AMP-activated protein kinase-related kinase NUAKI and that inhibition of miR-211 resulted in increased NUAK1 expression and reduced adhesion [24]. [score:7]
Expression level of discovered targets and correlation with miR-211 expression were analyzed in EOC tissues. [score:7]
As expected, we found that Cyclin D1 and CDK6 were downregulated in vivo by miR-211 and that EOC tumor growth was reduced significantly by miR-211 overexpression. [score:6]
Our previous data suggests that miR-211 inhibits EOC cell proliferation and that Cyclin D1 and CDK6 are direct targets of miR-211. [score:6]
Taken together, these results indicate that miR-211 can repress the expression of Cyclin D1 and CDK6 in EOC by directly targeting the 3′UTR of Cyclin D1 and CDK6 mRNA. [score:6]
When we overexpressed Cyclin D1 and CDK6 in miR-211 -overexpressing cells, miR-211 -induced cell cycle arrest and apoptosis were completely abrogated (Figure  6C and D). [score:5]
On this basis, it is possible that miR-211 -mediated inhibition of CDK6 expression in EOC could be a useful epigenetic therapeutic approach, although further experiments would be required to determine this. [score:5]
org, Targetscan and miRWalk databases to predict potential miR-211 targets. [score:5]
In the present study, we performed a database search for miR-211 expression in human ovarian cancer tissues compared to healthy control tissue, and found that miR-211 was significantly downregulated in clear-cell and high-grade serous carcinomas. [score:5]
We performed in vivo experiments to confirm our in vitro results that suggested that miR-211 inhibited EOC cell proliferation by targeting Cyclin D1 and CDK6. [score:5]
These in vivo results further indicated that miR-211 inhibits EOC growth and reduces Cyclin D1 and CDK6 expression. [score:5]
Spearman correlation analysis revealed a reverse correlation between miR-211 expression and Cyclin D1 or miR-211 and CDK6 expression (Figure  4G, H). [score:5]
Using bioinformatics, we identified several miR-211 targets and confirmed with luciferase assay that miR-211 directly binds to sequences in Cyclin D1 and CDK6 mRNA, repressing their translation into protein. [score:5]
Figure 1 miR-211 is downregulated in epithelial ovarian cancer (EOC) tissues and cell lines. [score:4]
Searching the literature, we found that miR-211 is downregulated in OC tissues [9]. [score:4]
A luciferase reporter system was developed to assess miR-211 regulation of the predicted targets. [score:4]
Cyclin D1 and CDK6 are direct target of miR-211. [score:4]
To demonstrate that miR-211 regulates cell proliferation through Cyclin D1 and CDK6, we tested whether Cyclin D1 and CDK6 could rescue the impaired proliferative phenotype in miR-211 overexpressing OVCAR3 and S KOV3 cells. [score:4]
Conversely, others reported that in oral carcinoma, miR-211 is upregulated, contributes to progression of oral carcinoma and correlates with poor prognosis in oral carcinoma [26]. [score:4]
miR-211 is downregulated in EOC tissues and cell lines. [score:4]
The authors suggested that rescuing miR-211 expression could have therapeutic applications. [score:3]
These results suggest that miR-211 inhibits EOC cell proliferation and induces apoptosis. [score:3]
A suspension of OVCAR3 cells (1 × 10 [7]) stably expressing miR-211 or cells infected with miR-Ctrl were injected subcutaneously into the left flank of each group. [score:3]
G- H. The mRNA expression levels of Cyclin D1 (G) or CDK6 (H) correlated inversely with miR-211. [score:3]
The results indicate that miR-211 inhibited proliferation, while Cyclin D1 or CDK6 partly, and Cyclin D1 + CDK6 almost completely restored cell proliferation (Figure  5B-F). [score:3]
Figure 2 miR-211 inhibits EOC cell proliferation. [score:3]
A. Nude mice were implanted with OVCAR3 cells stably expressing miR-Ctrl or miR-211. [score:3]
Finally, in vitro investigation confirmed that miR-211 is a tumor suppressor that controls Cyclin D1 and CDK6 expression. [score:3]
A. Schematic representation showing the five predicted miR-211 targets (TCF4, Cyclin D1, Cyclin D2, Cyclin D3 and CDK6) screened using three algorithms (miRNA. [score:3]
We further used a public data base to investigate miR-211 expression in EOC tissues and found that the of miR-211 expression was significantly lower in clear-cell OC (CCOC, n = 9) and high-grade serous ovarian carcinomas (HGSC, n = 12) than in ovarian surface epithelial cells (OSES, n = 9) (Figure  1A, GSE47841, p < 0.001) [27]. [score:3]
Next, we explored this finding in clinical samples by comparing miR-211 expression in normal epithelial ovarian tissues with primary EOC tissues. [score:3]
Consistent with the mentioned literature, miR-211 expression was significantly lower in EOC tissues than in normal epithelial ovarian tissues (Figure  1B, p < 0.01). [score:3]
miR-211 inhibits proliferation and induces apoptosis of EOC cells. [score:3]
D. Expression of miR-211 in LV-miR-211 or LV-miR-Ctrl transfected OVCAR3 and S KOV3 cells. [score:3]
We first constructed a miR-211 lentiviral vector (LV-miR-211), then infected OVCAR3 and S KOV3 cells with LV-miR-211 to establish stably expressing miR-211 cells (Figure  2D). [score:3]
OVCAR3 cells stably expressing miR-211 or control cells were injected subcutaneously into mice in each group. [score:3]
We inserted TCF4, CDK6, Cyclin D1, Cyclin D2 and Cyclin D3 3′UTR into luciferase reporter vectors and co -transfected with miR-211 expression plasmid into OVCAR3 and S KOV3 cells (Figure  4A). [score:3]
These results together demonstrate that miR-211 affects EOC cell proliferation, at least in part, through suppression of Cyclin D1 and CDK6. [score:3]
To confirm that Cyclin D1 and CDK6 are specifically targeted by miR-211, OVCAR3 and S KOV3 cells transfected with miR-211 or infected with LV-miR-211 were subjected to western blot analysis. [score:3]
Figure 5 miR-211 affects EOC cell proliferation through suppression of Cyclin D1 and CDK6. [score:3]
The data revealed that miR-211 targets two sites in Cyclin D1 and CDK6 (Additional file 1: Figure S1C-D). [score:3]
As shown in Figure  2B, miR-211 significantly inhibited EOC proliferation. [score:3]
The human miR-211 precursor sequences were cloned into the lentivirus based expression plasmid pSILK (Addgene, Cambridge, MA). [score:3]
Finally, OVCAR3 stably expressing miR-211 or control cells were injected subcutaneously into mice to determine in vivo effect of miR-211 on tumorigenesis. [score:3]
1: miR-211 targets multiple sites of Cyclin D1 and CDK6 3′UTR. [score:3]
Further in vitro investigations showed that miR-211 affected EOC cell proliferation and apoptosis through suppressing the expression of Cyclin D1 and CDK6. [score:3]
miR-211 affects ovarian cell proliferation and apoptosis through suppression of Cyclin D1 and CDK6. [score:3]
miR-211 was found to arrest cells in the G0/G1-phase, inhibit proliferation and induce apoptosis. [score:3]
Figure 4 Cyclin D1 and CDK6 are miR-211 targets. [score:3]
To quantitate miR-211 expression, total RNA was polyadenylated and reverse transcribed using the TaqMan MicroRNA Reverse Transcription Kit and TaqMan miRNA assay (Applied Biosystems, Foster City, CA), according to the manufacturer’s instructions. [score:2]
Figure 6 miR-211 regulates EOC cell cycle and cell apoptosis via repression of Cyclin D1 and CDK6. [score:2]
Furthermore, we performed cell cycle assays and found that Cyclin D1 or CDK6 partly rescued the cell proliferation that had been inhibited by miR-211 (Figure  6A). [score:2]
E. in OVCAR3 and S KOV3 cells stably expressing miR-211 compared to control cells. [score:2]
A. Expression of miR-211 was lower in clear cell ovarian carcinomas (CCOC, n = 9) and high-grade serous ovarian carcinomas (HGSC, n = 12) compared to ovarian surface epithelial cells (OSEC, n = 9) (GSE47841, p < 0.001). [score:2]
MiR-211 overexpression led to more cell apoptosis, while Cyclin D1 and CDK6 each significantly reduced apoptosis (Figure  6B). [score:2]
PERK is important to survival of tumor and normal cells in response to stress [18- 22] and Chitnis et al. [17] suggested that miR-211 negatively regulates chop accumulation, allowing cells to re-establish homeostasis before having to commit to apoptosis. [score:2]
The present study investigated the regulatory role and implications of aberrant expression of miR-211 in epithelial OC (EOC). [score:2]
miR-211 is known to be dysregulated in ovarian cancer: however, its function and the downstream effect of its loss-of-function in ovarian cancer have not been described before. [score:2]
As shown in Figure  3B, miR-211 transfected cells had a higher incidence of apoptosis than miR-211-Ctrl transfected cells. [score:1]
B. Apoptosis analysis of OVCAR3 and S KOV3 cells transfected with LV-miR-Ctrl, LV-miR-211, LV-miR-211 + Cyclin D1 or LV-miR-211 + CDK6 plasmids. [score:1]
B. Cell counting of OVCAR3 and S KOV3 cells transfected with LV-miR-Ctrl, LV-miR-211, LV-miR-211 + Cyclin D1 or LV-miR-211 + CDK6 plasmids. [score:1]
was performed to examine Cyclin D1 and CDK6 levels in cells transfected with LV-miR-Ctrl, LV-miR-211, LV-miR-211 + Cyclin D1 and LV-miR-211 + CDK6 (Figure  5A). [score:1]
The full-length 3′UTR of Cyclin D1 and CDK6 gene containing the putative miR-211 biding sites was amplified by PCR and was inserted into the pGL3 vector subcloned with CMV promoter (Promega, Madison, WI). [score:1]
Both genes have two potential complementary miR-211 binding sites (Figure  4C, D). [score:1]
Figure 7 miR-211 reduces EOC tumorigenesis in vivo. [score:1]
miR-211 reduces EOC tumorigenesis in vivo. [score:1]
A. of Cyclin D1 and CDK6 levels in OVCAR3 and S KOV3 cells transfected with LV-miR-Ctrl, LV-miR-211, LV-miR-211 + Cyclin D1 or LV-miR-211 + CDK6 plasmids. [score:1]
D. Apoptosis analysis of OVCAR3 and S KOV3 cells transfected with LV-miR-Ctrl, LV-miR-211 or LV-miR-211 + Cyclin D1 + CDK6 plasmids. [score:1]
A. of OVCAR3 and S KOV3 cells tranfected with LV-miR-Ctrl, LV-miR-211, LV-miR-211 + Cyclin D1 or LV-miR-211 + CDK6 plasmids. [score:1]
CDK6 Cyclin D1 Epithelial ovarian cancer miR-211 Ovarian cancer (OC) has a high mortality rate and low 5-year survival rate due to lack of early, safe and non-invasive detection methods. [score:1]
We observed that Cyclin D1 and CDK6 staining in LV-miR-211 group was weaker than in the control group (Figure  7D). [score:1]
A. of OVCAR3 and S KOV3 cells transfected with miR-211 or miR-Ctrl. [score:1]
C. of OVCAR3 and S KOV3 cells tranfected with LV-miR-Ctrl, LV-miR-211 or LV-miR-211 + Cyclin D1 + CDK6 plasmids. [score:1]
C- D. Sequence of miR-211 with the putative binding sites of Cyclin D1 (C) and CDK6 (D) 3′ UTR. [score:1]
Next, we performed cell cycle analysis and noted that miR-211 transfection significantly arrested significantly more cells in the G0/G1 phase (Figure  3A) than miR-211-Ctrl transfection. [score:1]
Plasmids inserted into the Renilla lucifearse vector (Promega) with Cyclin D1 or CDK6 3′UTR inserts were co -transfected with miR-Ctrl or miR-211 plasmids. [score:1]
D. of Cyclin D1 and CDK6 levels in OVCAR3 and S KOV3 cells transfected with LV-miR-Ctrl, LV-miR-211 or LV-miR-211 + Cyclin D1 + CDK6 plasmids. [score:1]
We further investigated the significance of miR-211 expression in EOC in vitro and found that miR-211 significantly modulated EOC cell proliferation and colony formation. [score:1]
B. OVCAR3 cells were co -transfected with TCF4, CDK6, Cyclin D1, Cyclin D2 or Cyclin D3 3′UTR pGL plasmid with miR-211. [score:1]
As expected, miR-211 significantly reduced colony numbers to 20% in both EOC cell lines (Figure  2E). [score:1]
Cell cycle analysis showed that miR-211 arrested cells in the G0/G1 phase, resulting in apoptosis. [score:1]
Cyclin D1 and CDK6 appear to be key players in EOC tumorigenesis, and our discovery of correlated expression of miR-211 and CDK6/Cyclin D1 provides new insight that presents tentative methods for diagnosis, prognosis and therapy for EOC, and a rational for further investigation into the potential use of miR-211 for diagnosis and therapy. [score:1]
E. of Cyclin D1 and CDK6 levels in OVCAR3 and S KOV3 cells transfected with miR-211 or miR-Ctrl. [score:1]
D. of Cyclin D1 and CDK6 staining in LV-miR-Ctrl and LV-miR-211 groups. [score:1]
E. Cell counting of OVCAR3 and S KOV3 cells transfected with LV-miR-Ctrl, LV-miR-211 or LV-miR-211 + Cyclin D1 + CDK6 plasmids. [score:1]
We analyzed miR-211 expression in clinical samples of primary EOC tissues compared to normal epithelial ovarian tissues and in the EOC cell lines: OVCAR3, Caov3, OVCA429, S KOV3 and A2780 compared to human ovarian surface epithelial cells. [score:1]
We extended our investigations to six EOC cell lines (OVCAR3, Caov3, OVCA429, S KOV3, A2780 and COV644) and found that their miR-211 expression levels were significantly lower than those of human ovarian surface epithelial (HOSE) cells (Figure  1C). [score:1]
A. miR-211 levels in OVCAR3 and S KOV3 cells transfected with miR-211 or miR-Ctrl. [score:1]
The microRNA miR-211 is localized on intron 6 of the Trpm1 gene at 15q13-q14, a locus that is frequently lost in neoplasms. [score:1]
The microRNA miR-211 is localized on intron 6 of the Trpm1 gene at 15q13-q14, a locus that is frequently lost in neoplasms [13- 16]. [score:1]
B. Apoptosis analysis of OVCAR3 and S KOV3 cells transfected with miR-Ctrl or miR-211. [score:1]
Oligonucleotides including miR-211 miRNA, mimics and non-specific miRNA negative control (miR-Ctrl) [53] were synthesized and purified by GenePharma (Shanghai). [score:1]
Figure 3 miR-211 arrests EOC cell cycle and induces apoptosis. [score:1]
F. of Cyclin D1 and CDK6 levels in OVCAR3 and S KOV3 cells transfected with LV-miR-211 or LV-miR-Ctrl. [score:1]
B. OVCAR3 and S KOV3 cells were transfected with miR-211 or miR-Ctrl for 48 hours, then seeded in 24-well plates (0.25 × 10 [4] cells/well). [score:1]
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2
[+] score: 271
Other miRNAs from this paper: mmu-mir-21a, mmu-mir-22, mmu-mir-29a, mmu-mir-21b, mmu-mir-21c
In the miR-211 inhibitors group, the miR-211 expression and the mRNA expressions of Bax and p53 decreased, while the SIRT1 and Bcl-2 expression significantly increased; the miR-211 expression in the miR-211 inhibitors + siRNA-SIRT1 group decreased but there were no obvious changes in the expressions of Bax, p53, SIRT1, and Bcl-2 (P>0.05). [score:15]
Compared with the blank and NC groups, the expressions of Bax and p53 proteins in the miR-211 mimics and siRNA-SIRT1 groups increased (P<0.05), while the expressions of SIRT1 and Bcl-2 decreased (P<0.05); the protein expressions of Bax and p53 in the miR-211 inhibitors group decreased and the expressions of SIRT1 and Bcl-2 increased (P<0.05); no significant change was observed in the protein expressions of SIRT1, Bcl-2, Bax, and p53 in the miR-211 inhibitors + siRNA-SIRT1 group (P>0.05). [score:14]
Figure 3Expression of miR-211 and mRNA and protein expressions of SIRT1, Bcl-2, Bax, and p53 in lens tissues of mice(A) miR-211 expression and mRNA and protein expressions of SIRT1, Bcl-2, Bax, and p53 in mice lens; (B) strip chart of SIRT1, Bcl-2, Bax, and p53 proteins; (C) expressions of SIRT1, Bcl-2, Bax, and p53 proteins in mice lens; *, P<0.05 compared with the normal group. [score:10]
miR-211 expression and mRNA expressions of SIRT1, Bcl-2, Bax, and p53 in each groupIn comparison with the normal group, the expressions of miR-211, Bax, and p53 in the other groups increased prominently, while the expressions of SIRT1 and Bcl-2 decreased significantly (P<0.05). [score:9]
In comparison with the normal group, an increase in the protein expressions of Bax and p53 and a decrease in the expressions of SIRT1 and Bcl-2 was observed in the blank group, NC group, miR-211 mimics group, miR-211 inhibitors group, siRNA-SIRT1 group, and miR-211 inhibitors + siRNA-SIRT1 group (P<0.05). [score:9]
The cells were assigned into the normal group, blank group (without any transfection sequence), negative control (NC) group (transfected with miR-211 negative control sequence), miR-211 mimics group (transfected with miR-211 mimics), miR-211 inhibitors group (transfected with miR-211 inhibitors), siRNA-SIRT1 group (transfected with siRNA-SIRT1), miR-211 inhibitors + siRNA-SIRT1 group (transfected with miR-211 inhibitors and siRNA-SIRT1). [score:9]
Expressions of miR-211, SIRT1, Bcl-2, Bax, and p53 in lens tissues of mice in the normal and mo del groupsIn the diabetic cataract group, miR-211 expression and mRNA expressions of Bax and p53 significantly increased (P<0.05) and the mRNA expressions of SIRT1 and Bcl-2 obviously decreased (P<0.05) compared with the normal group (Figure 3A). [score:8]
Compared with the blank and NC groups, the miR-211 expression in the miR-211 mimics group increased (P<0.05); there was no significant change in the miR-211 expression in the siRNA-SIRT1 group (P>0.05); the mRNA expressions of Bax and p53 in the miR-211 mimics and siRNA-SIRT1 groups increased (P<0.05); the mRNA expressions of SIRT1 and Bcl-2 decreased significantly (P<0.05). [score:8]
Additionally, our results found that miR-211 could inhibit the proliferation of lens epithelial cells and promote cataract development by suppressing the expression of SIRT1 gene. [score:8]
U6 was set as the internal reference for the relative expression of miR-211 and β-actin for the relative expressions of SIRT1, Bcl-2, Bax, and p53; and 2−ΔΔ C [t] indicated a ratio of gene expression between the experimental group and the control group, and the formula was as follows: ΔΔ C [T] = Δ C [t] (case group) – Δ C [t] (control group), Δ C [t] = C [t] [miRNA] – C [t] [β-actin]. [score:7]
In our study, we observed that inhibiting the miR-211 expression could stimulate the expression of anti-apoptotic protein Bcl-2 in lens epithelial cells of diabetic cataract mice. [score:7]
Meanwhile, our study also proved that the inhibition of miR-211 expression could upsurge the expression of anti-apoptotic protein Bcl-2 of lens epithelial cells in diabetic cataract mice. [score:7]
To conclude, our observations demonstrated that miR-211 was highly expressed in lens epithelial cells of diabetic cataract mice, and it participated in the regulation of cell apoptosis and proliferation by targetting SIRT1 gene. [score:6]
In the diabetic cataract group, miR-211 expression and mRNA expressions of Bax and p53 significantly increased (P<0.05) and the mRNA expressions of SIRT1 and Bcl-2 obviously decreased (P<0.05) compared with the normal group (Figure 3A). [score:6]
In the present study, we observed a higher miR-211 expression and lower SIRT1 expression in diabetic mice than normal mice. [score:5]
In comparison with the miR-211 inhibitors group, the proliferation activity in the miR-211 inhibitors + siRNA-SIRT1 group decreased remarkably (P<0.05) (Figure 7). [score:5]
In comparison with the normal group, the expressions of miR-211, Bax, and p53 in the other groups increased prominently, while the expressions of SIRT1 and Bcl-2 decreased significantly (P<0.05). [score:5]
miR-211 expression and mRNA expressions of SIRT1, Bcl-2, Bax, and p53 in each group. [score:5]
To verify if SIRT1 is the direct target gene of miR-211, luciferase reporter vector wild-type- miR-211/SIRT1 and mutant- miR-211/SIRT1 recombinant plasmids were added with 3′-UTR wild sequence of SIRT1 after which a mutation sequence was established. [score:5]
In addition, we observed that in comparison with the blank and NC groups, expressions of Bax and p53 proteins increased in the miR-211 mimics and siRNA-SIRT1 groups, while they decreased in the miR-211 inhibitors group. [score:5]
The apoptosis rate in the miR-211 inhibitors + siRNA-SIRT1 group was higher than the miR-211 inhibitors group (P<0.05) (Figure 9). [score:5]
showed the cell percentages in the blank group, NC group, miR-211 mimics group, miR-211 inhibitors group, siRNA-SIRT1 group, and miR-211 inhibitors + siRNA-SIRT1 group significantly increased in the G [0]-phase, but decreased in S-phase and G [2]-phase (P<0.05) in contrast with the normal group. [score:5]
A total of 100 pmol miR-211 mimics, miR-211 100 inhibitors, siRNA-SIRT1, miR-211 inhibitors + siRNA-SIRT1, and negative control (the final concentration added into cells was 50 nm) were diluted by 250 μl serum-free Opti-MEM medium (31985, Gibco Company, U. S. A. ), mixed gently and incubated at room temperature for 5 min. [score:5]
Our results mainly demonstrated that inhibiting the miR-211 expression could diminish the rate of apoptosis of lens epithelial cells in diabetic cataract mice whereas silencing the SIRT1 gene could stimulate the rate of apoptosis of lens epithelial cells in diabetic cataract mice. [score:5]
PI single staining showed the cell percentages in the blank group, NC group, miR-211 mimics group, miR-211 inhibitors group, siRNA-SIRT1 group, and miR-211 inhibitors + siRNA-SIRT1 group significantly increased in the G [0]-phase, but decreased in S-phase and G [2]-phase (P<0.05) in contrast with the normal group. [score:5]
Double showed that in comparison with the normal group the apoptosis rate in the blank group, NC group, miR-211 mimics group, miR-211 inhibitors group, siRNA-SIRT1 group, and miR-211 inhibitors + siRNA-SIRT1 group increased significantly (P<0.05). [score:5]
Expression of miR-211 and mRNA and protein expressions of SIRT1, Bcl-2, Bax, and p53 in lens tissues of mice. [score:5]
Compared with the blank group and NC group, the cell percentage in the G [1]-phase increased significantly in the miR-211 mimics group and siRNA-SIRT1 group while being decreased at S-phase and G [2]-phase (P<0.05); the cell percentage in the miR-211 inhibitors group significantly declined at G [1]-phase, but increased at S- and G [2]-phases (P<0.05); no obvious changes in cell percentages were observed in G [1]-, S-, and G [2]-phases in the miR-211 inhibitors + siRNA-SIRT1 group (P>0.05). [score:4]
Therefore, we hypothesized that SIRT1 could be a novel target gene of the miRNA member miR-211 in diabetic cataract and the present study aimed at investgating the effects of miR-211 on the proliferation and apoptosis of lens epithelial cells in diabetic cataract mice by regulating the SIRT1 gene. [score:4]
The qRT-PCR results indicated that miR-211 was highly expressive in lens epithelial cells of diabetic cataract mice and SIRT1 was weakly positive and was not highly expressed in the mo del group compared with the normal group. [score:4]
A recent study demonstrated that expression of miR-211 increased after down -regulating the level of Bcl-2 [47]. [score:4]
Site-directed mutagenesis method was conducted using a bioinformatics software to predict the binding site of miR-211 and its target gene SIRT1. [score:4]
Likewise, our study showed that miR-211 -induced Bcl-2 up-regulation was linked to apoptosis of diabetic cataract cells. [score:4]
The cells percentage in G [1]-phase was increased significantly but decreased in S- and G [2]-phases in the miR-211 inhibitors + siRNA-SIRT1 group was higher compared with the value observed in the miR-211 inhibitors group (P<0.05) (Figure 8). [score:4]
The verification of the targetting relationship between miR-211 and SIRT1. [score:3]
Our study showed that miR-211 could promote the apoptosis of lens epithelial cells via targetting SIRT1 gene. [score:3]
MiR-211 belongs to a group of specific miRNAs that are highly expressed in human vitreous [21]. [score:3]
org was employed to analyze the target genes of miR-211, and a dual luciferase reporter gene assay was performed to verify whether SIRT1 was a direct gene of miR-211. [score:3]
miR-211 specifically targeted SIRT1. [score:3]
Relative mRNA expressions of miR-211, Bax, p53, SIRT1, and Bcl-2 in each group. [score:3]
The exact mechanism underlying how miR-211 affects lens epithelial cells in diabetic cataract mice by targetting SIRT1 gene needs to be studied in depth in the future. [score:3]
In comparison with the blank group and NC group, cell proliferation activity in the miR-211 mimics group and siRNA-SIRT1 group decreased while cell proliferation in the miR-211 inhibitors group increased appreciably (P<0.05). [score:3]
miR-211 specifically targeted SIRT1According to the results from biological website www. [score:3]
One study detected that the miR-211 expression in colorectal cancer tissues decreased the apoptosis of colorectal cancer cells by stable gene transfection technology [49]. [score:3]
The apoptosis rate in the miR-211 mimics group and siRNA-SIRT1 group increased (P<0.05) though it declined in the miR-211 inhibitors group (P<0.05). [score:3]
No significant changes in cell proliferation were observed in the miR-211 inhibitors + siRNA-SIRT1 group (P>0.05). [score:3]
org, SIRT1 was the target gene of miR-211 (Figure 4A). [score:3]
Expressions of miR-211, SIRT1, Bcl-2, Bax, and p53 in lens tissues of mice in the normal and mo del groups. [score:3]
Thus, miR-211 might be a novel underlying target for the treatment of diabetic cataract. [score:3]
Figure 4The verification of the targetting relationship between miR-211 and SIRT1(A) Sequence of 3′-UTR region of SIRT1 mRNA binding with miR-211; (B) luciferase activity detection; *, P<0.05 compared with the NC group. [score:2]
Compared with the blank group and NC group, no apparent changes were observed in the apoptosis rate in the miR-211 inhibitors + siRNA-SIRT1 group (P>0.05). [score:2]
Likewise, the study showed that in comparison with the normal group, the apoptosis index of the lens tissues increased significantly in the diabetic cataract group, which clearly indicated that miR-211 could promote the apoptosis of lens epithelial cells in diabetic cataract mice. [score:1]
Therefore, it can be concluded that miR-211 can specifically bind to the SIRT1 gene. [score:1]
MiR-211 mimics and miR-211 NC were respectively transfected with luciferase reporter vector into HEK-293T cells (CRL-1415, American Type Culture Collection (ATCC), U. S. A. ). [score:1]
Various miRNAs have been observed to exhibit ocular enrichment, including miR-211 [35]. [score:1]
Figure 5Relative mRNA expressions of miR-211, Bax, p53, SIRT1, and Bcl-2 in each group*, P<0.05 compared with the normal group; [#], P<0.05 compared with the blank and NC groups. [score:1]
In our study, we investigated the influence of miR-211 on the proliferation and apoptosis of lens epithelial cells in diabetic cataract mice by targetting the SIRT1 gene. [score:1]
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3
[+] score: 224
Figure 2 (A) miR-211 mimics can enhance the expression of miR-211 and miR-211 inhibitor can repress the expression of miR-211 in the HepG2 cells. [score:7]
In addition, analysis also showed that ectopic expression of miR-211 markedly suppressed STAB2 expression in HepG2 cell line (Figure 4C and 4D). [score:7]
Figure 3 (A) Upexpression of miR-211 can significantly promoted the HepG2 cells invasion whereas miR-211 inhibitor inhibitedHepG2cell invasion. [score:7]
Upregulation of miR-211 inhibits cell invasion. [score:6]
Upregulation of mir-211 inhibits cell invasion. [score:6]
Our study showed that miR-211 expression was downregulated in HCC cells and HCC tissues. [score:6]
Upregulation of miR-211 inhibits cell proliferation. [score:6]
These results suggested that miR-211 might act as a tumor suppressor whose down-regulation contributed to the progression and metastasis of HCC. [score:6]
As for the mechanism, our results indicated that miR-211 directly targeted SATB2 to inhibit cell proliferation and invasion in HCC cells. [score:6]
Furthermore, enforced expression of miR-211 promoted tumor cell growth at least in part by down -regulating the CHD5 tumor suppressor [31]. [score:6]
MiR-211 was upregulated in oral carcinoma and higher miR-211 expression was associated with nodal metastasis, vascular invasion, and poor prognosis of oral carcinoma [32]. [score:6]
Overexpression of miR-211 can promote the invasion of HepG2 cells and SMMC7721 compared with the control whereas miR-211 inhibitor inhibited cell invasion (Figure 3A and 3B). [score:6]
As expected, the ectopic expression of SATB2rescued the miR-211 -mediated inhibition of cell proliferation and migration in HepG2 cells (Figure 5C and 5D). [score:5]
The ectopic expression of SATB2 rescued the miR-211 -mediated inhibition of cell proliferation in HepG2 cells. [score:5]
As shown in Figure 1D, the expression of miR-211 was significantly down-regulated in four cell lines (MHCC-97H, QGY-7703, SMMC7721 and HepG2) compared with one liver adenocarcinoma cell line, SK-Hep-1, and two adjacent non-neoplastic tissues. [score:5]
To study the role of miR-211 in HCC development, SMMC7721 and HepG2 were transfected with miR-211 mimics or inhibitor with high transfection efficiency (Figure 2A and 2B). [score:4]
miR-211 is downregulated in HCC cell lines and tissues. [score:4]
In our research, the tumor-suppressive role of miR-211 in vivo was treated through direct miRNA mimics injection. [score:4]
Down expression of miR-211 inhibited the growth rate of HCC cells compared with control cells in both SMMC7721 and HepG2 cells (Figure 2C and 2D). [score:4]
miR-211 regulated cell proliferation and invasion through inhibiting SATB2. [score:4]
STAB2 is a direct target of miR-211. [score:4]
Researchers have illustrated that miR-211 is abnormally expressed in various tumors and directly involves in human cancer processes, such as cell proliferation, migration and metastasis [31– 36]. [score:4]
MiR-211 mimics/inhibitors and negative control molecules (scramble control mimic and inhibitor) and pcDNA-SATB2 were purchased from Dharmacon (Austin, TX, USA). [score:4]
stab2 is a direct target of mir-211. [score:4]
Overexpression of miR-211 reduced SATB2 both mRNA and protein levels in HCC cells. [score:3]
MiR-211 is downregulated in HCC cell lines and tissues. [score:3]
Figure 1 (A) qRT-PCR analysis of miR-211 expression in 40 pairs HCC tissues and their corresponding no tumor tissues. [score:3]
Our results indicated that miR-211 was down-regulated in HCC tissues compared with adjacent non-neoplastic tissues. [score:3]
These results demonstrate thatSATB2 is a functional target gene of miR-211 in HCC. [score:3]
Our result proved that miR-211 significantly inhibited the growth of HCC cells. [score:3]
Furthermore, over -expression of miR-211 could repress HCC cell proliferation and invasion. [score:3]
Moreover, SATB2 rescued the miR-211 -mediated inhibition of cell invasion and proliferation and there was an inverse correlation between miR-211 and SATB2 levels in HCC tissues. [score:3]
On the other hand, another study showed that miR-211 was a suppressor of melanoma invasion during human melanoma progression [34, 37, 38]. [score:3]
Integrating bioinformatics and experimental assays, we identified SATB2 as a direct downstream target of miR-211 in HCC cells. [score:3]
Using bioinformatics analysis, we found that 3′-UTR of STAB2 contained a conserved putative target site for miR-211 (Figure 4A). [score:3]
Figure 4 (A) Predicted miR-211 target sequence in the 3′UTR of STAB2 and mutant containing 8 altered nucleotides in the 3′UTR of STAB2. [score:3]
miR-211 inhibited the growth of HepG2-engrafted tumors. [score:3]
Meanwhile, miR-211 repressed the mRNA expression of STAB2. [score:3]
Moreover, enforced miR-211 expression increased the proliferation, migration, and anchorage-independent colony formation of oral carcinoma cells. [score:3]
Furthermore, ectopic expression of miR-211 repressed the proliferation and invasion of HCC cells. [score:3]
Conversely, miR-211 inhibitor significantly promoted the proliferation of the SMMC7721 cells. [score:3]
analysis in randomly selected xenograft mouse tumors showed that miR-211 mimics-injecting tumors expressed lower levels of STAB2 than scramble controls (Figure 7E). [score:3]
Importantly, SATB2 rescued the miR-211 -mediated inhibition of cell invasion and proliferation. [score:3]
As shown in Figure 1B, the expression of miR-211 in HCC tissues was lower than in adjacent tissues (Figure 1B, p < 0.001). [score:3]
The expression of miR-211 was normalized to U6 snRNA. [score:3]
Conversely, miR-211 inhibitor significantly promoted the proliferation of the HepG2 cells. [score:3]
In conclusion, we identified that miR-211 acted a tumor suppressive miRNA in HCC tumorigenesis and progression. [score:3]
STAB2 was inversely expressed with miR-211 in HCC patients. [score:3]
Given that reintroduction of miR-211 inhibited tumor formation in xenograft mo del, this mature miRNA could serve as a potential therapeutic strategy for HCC. [score:3]
Further western blot analysis demonstrated the negative regulation of miR-211 to SATB2. [score:2]
Moreover, tissues from lymph node metastases also expressed lower levels of miR-211 compared with primary HCC tissues and the adjacent normal tissue (Figure 1C). [score:2]
Mutation of miR-211 binding site from the STAB2 3′-UTR largely abolished the effects of miR-211 mimics. [score:2]
Moreover, tissues from lymph node metastases expressed lower levels of miR-211 compared with primary HCC tissues and the adjacent normal tissue, indicating an inverse relationship between miR-211 and the metastatic status of HCC. [score:2]
These results suggest that miR-211 might be a potential therapeutic choice in HCC. [score:1]
In this study, we aimed to determine the expression and function of miR-211 in HCC and investigate the molecular mechanism of miR-211 in the initiation and progression of HCC. [score:1]
Moreover, miR-211 decreased the luciferase reporter activity of wild-type 3′UTR but not mutant 3′UTR of SATB2. [score:1]
To our knowledge, there is no study on miR-211 and HCC tumorigenicity in a xenograft mo del. [score:1]
These findings suggest that miR-211 may play an important role in promoting carcinogenesis of HCC. [score:1]
To our knowledge, the role and mechanism of miR-211 in HCC have not been completely understood. [score:1]
Conversely, miR-211 mimics promoted the proliferation of the HepG2 cells in both SMMC7721 and HepG2 cells (Figure 2C and 2D). [score:1]
Cells in 24-well plates (50% confluency) were co -transfected with miR-211 mimic (20 nM) and STAB2 3′UTR Reporter (200 ng). [score:1]
As shown in Figure 4B, miR-211 mimics repressed the luciferase activity. [score:1]
Moreover, our investigation for the expression of SATB2 and miR-211 in 20HCC patients indicated that there was an inverse correlation between miR-211 and SATB2 levels. [score:1]
miR-211 repressed the growth of HepG2-engrafted tumors. [score:1]
Comparison of miR-211 levels and levels corresponding to STAB2 in HCC exhibited inverse correlation between STAB2 and miR-211 (r [2] = 0.426, p = 0.0018) (Figure 6E). [score:1]
In agreement with the tumor growth curve, the volumes and weights of tumors treated by miR-211 mimics were also lower than scrambled mimics -treated tumors (Figure 7B and 7C). [score:1]
Complementary sequence of miR-211 was identified in the 3′UTR of SATB2 mRNA. [score:1]
Figure 7 (A) Representative tumors were photographed at 15 days after the first treatment with miR-211 mimic or scramble. [score:1]
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4
[+] score: 173
Using a set of Apc-mutant ESCs harbouring different levels of Wnt signaling, we found that, among others, down-regulation of Tcf3, a key member of the pluripotency circuit, as well as induction of a novel Wnt-regulated microRNA, miR-211, represent two important downstream effects through which Wnt signaling inhibits neural differentiation in mouse ESCs. [score:7]
On the other hand, microRNAs usually exert their function by targeting multiple genes and it is plausible that miR-211 inhibits early neural differentiation in mESCs by repressing target genes other than Tcf3. [score:7]
We suggest that Wnt signaling represses Tcf3 expression possibly by altering the histone marks at the Tcf3 promoter and by activating miR-211 expression, thus extending our understanding of Tcf3 regulation in stem cells. [score:6]
Notably, these modifications occur shortly after Wnt stimulation and it is plausible to think that the chromatin modifications within the Tcf3 locus can trigger the downregulation process of Tcf3 expression which can be stabilized further on via miR-211 function. [score:6]
Accordingly, miR-211 has also been shown to play a key role in melanoma tumor formation and metastasis, as well as mesenchymal to epithelial transition (MET) [53], [54], [55] Taken together, we have revealed two downstream effects of Wnt signaling which contribute to the differentiation defects observed upon constitutive activation of canonical Wnt signaling, namely downregulation of Tcf3 expression and induction of miR-211. [score:6]
B. Histogram showing relative expression of selected miR-211 predicted targets in wild type ESCs treated with Wnt3a condition medium or L-medium for different time intervals. [score:5]
D. of the miR-211 predicted targets Sox11 and Sf3b1 in miR-211 over expressing cells and their wild type controls. [score:5]
miR-211, a novel Wnt-regulated microRNA, targets Tcf3 and attenuates early neural differentiation in wild-type ESCsIt has been previously shown that members of the core pluripotency circuit are fine-tuned via microRNA -mediated regulation in embryonic stem cells [33], [34], [35], [36], [37]. [score:5]
C. qRT-PCR analysis of miR-211 expression in wild type ESCs stably expressing miR-211 or the corresponding empty vector. [score:5]
The inhibitory effects of miR-211 were not observed when mutant forms of the 3′UTR, i. e. lacking 7 or 4 nucleotides of the miRNA seed sequence target (MTR1 and MTR2 respectively) were used (Figure 7F). [score:5]
Stable clones over expressing mmu-miR-211 were generated by transfecting Bruce4 wild type ESCs with miR-211 expressing plasmid pEZX-MR01 (Genecopoeia), or the corresponding empty vector. [score:5]
These results suggest that miR-211 functions at early stages of neural differentiation and its ectopic expression in wild type ES cells is not sufficient to inhibit further neural commitment as differentiation proceeds. [score:5]
In silico analysis with three software packages, namely Miranda [39], Targetscan [40] and PicTar [41], pointed to several potential miR-211 target genes predicted by all three programs. [score:5]
D. of Tcf3 expression in protein lysates isolated from independent clones of wild type ESCs stably expressing miR-211 (miR-211 OE) or the corresponding empty vector (control). [score:5]
To confirm that miR-211 directly targets Tcf3, we cloned the 3′ untranslated region (3′UTR) of the mouse Tcf3 gene in the pmirGLO reporter plasmid (Figure 7E) and performed a luciferase -based reporter assay. [score:5]
Histogram showing relative expression of selected miR-211 predicted targets in ApcNN and wild type ESCs. [score:5]
H. Histogram showing the relative expression of early neural markers Fgf5, Nestin, Pax6 and Sfrp2 in embryoid bodies derived from independent wild type ESCs clones stably expressing miR-211 or the corresponding empty vector. [score:5]
We also provide a more detailed picture on how Wnt signaling counteracts Tcf3 function in stem cells by showing that Tcf3 repression, in the context of active Wnt signaling, involves histone modifications at the Tcf3 promoter and the activation of miR-211, which post-transcriptionally stabilizes Tcf3 downregulation. [score:4]
Of the different candidate miRNAs induced upon Wnt activation, mmu-miR-211 showed a Wnt dosage -dependent up-regulation among the different Apc-mutant ESCs (Figure 7A). [score:4]
miR-211, a novel Wnt-regulated microRNA, targets Tcf3 and attenuates early neural differentiation in wild-type ESCs. [score:4]
A. qRT-PCR analysis showing a dosage -dependent up-regulation of miR-211 in different Apc-mutant ESCs. [score:4]
The Wnt-regulated miR-211 targets Tcf3 in mouse ESCs. [score:4]
qRT-PCR analysis showing a dosage -dependent up-regulation of miR-211 in different Apc-mutant ESCs. [score:4]
Accordingly, activation of Wnt signaling in wild type ESCs either by Wnt3a conditioned medium (CM) or by GSK3 inhibition, confirmed that miR-211 is a novel Wnt-regulated microRNA in mouse embryonic stem cells (Figure 7B and 7C). [score:4]
Transfection of HEK293 cells with the Tcf3-3′UTR reporter plasmid confirmed that Tcf3 is a direct target of miR-211 (Figure 7F). [score:4]
Altogether, our results indicate that miR-211, a novel Wnt-regulated miRNA, can fine-tune Tcf3 expression and attenuate early neural differentiation in wild type ESCs. [score:4]
As an additional regulatory mechanism, we also described a novel Wnt -induced micro RNA, miR-211, and demonstrated that it targets Tcf3 in ApcNN ESCs. [score:4]
Cells were co -transfected with 250 ng of UTR (or MTR) reporter plasmid and either mmu-miR-211 mimic or non-targetting oligos (40 nM, Dharmacon) using lipofectamin 2000 (Invitrogen). [score:3]
However, miR-211 over -expression in wild type ESCs does not reduce Tcf3 levels to the same degree as observed in ApcNN ES cells thus suggesting that multiple Wnt -mediated mechanisms are likely to exist. [score:3]
showed that, unlike Sox11 and Sf3b1 (Figure S7D), Tcf3 protein level was decreased upon miR-211 ectopic expression (Figure 7D). [score:3]
The observation that Wnt signaling induces miR-211 expression might also be of interest for other disciplines of research and in particular cancer. [score:3]
Sequence alignment between miR-211 and its target site on Tcf3-3′-UTR. [score:3]
F. HEK-293 cells were co -transfected with the Tcf3-3′-UTR luciferase vector, and either with miR-211 or a non -targeting miRNA. [score:3]
I. qRT-PCR analysis of Fgf5, Nestin, Pax6 and Sfrp2 in wild type ESCs stably expressing miR-211 or the corresponding empty vector, cultured for 24 h in N2B27 medium. [score:3]
Several stable ESC clones were generated which ectopically over-express miR-211 in an otherwise wild type background (Figure S7C). [score:3]
G. Flow cytometric analysis of Tuj1 and Nestin in miR-211 over expressing ESCs (miR-211 OE) and their controls (Emp) after 13 days of neural differentiation. [score:3]
FACS analysis for Tuj1, a marker for mature neurons and Nestin, revealed that both miR-211 over -expressing ES cells and their wild type controls give rise to similar number of neurons and neural progenitor cells after 13 days of in vitro differentiation, thus suggesting that miR-211 does not affect terminal neural differentiation. [score:3]
assay also confirmed that miR-211 does not suffice to inhibit neural differentiation (data not shown). [score:2]
We next assessed the differentiation potential of miR-211 over -expressing clones using in vitro neural differentiation assay as well as in vivo teratoma formation. [score:2]
Moreover, we show that Wnt -mediated repression of Tcf3 involves epigenetic regulation associated with histone modifications and Wnt -mediated induction of miR-211. [score:2]
To evaluate the role of miR-211 at earlier stages of differentiation, we derived embryoid bodies (EBs) from miR-211 over -expressing cells and their wild type controls and analyzed lineage differentiation at different time points. [score:1]
The Tcf3-3′-UTR plasmid was obtained by PCR amplification from mouse genomic DNA of a 565 bp fragment encompassing the Tcf3-3′-UTR inclusive of the miR-211 target site (forward primer 5′-AAATT GAGCTCTCCCCTTGCGCTGTGGTG-3′; reverse primer 5′-AAAAA CTCGAGGGTGGGGGAAGGGGCAGA-3′). [score:1]
qRT-PCR analysis for different lineage-specific markers indicated that, unlike mesodermal, endodermal and pluripotency markers (data not shown), early neuroectodermal differentiation was specifically attenuated by miR-211. [score:1]
RNAs were isolated at different time points and were subjected to qRT-PCR analysis of miR-211 or snoRNA-234 as an internal control. [score:1]
In line with our observation, a tumor promoting function has recently been described for miR-211 in colorectal cancer cells [52]. [score:1]
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5
[+] score: 166
After the transfection of miR-211-5p mimic or inhibitor, we found that neurons with the overexpression of miR-211-5p displayed significantly decreased growth and branching of longest neurite, whereas miR-211-5p inhibitor induced markedly increased branching but without the length change (Figures 3A–C). [score:7]
Although we found miR-211-5p inhibitor could not affect NUAK1 expression, miR-211-5p inhibitor alleviated the insult of Aβ on neurite growth and branching in our study. [score:7]
Our results showed that miR-211-5p was up-regulated and NUAK1 was down-regulated in both AD cell and mouse mo dels. [score:7]
To explore the dynamic changes of miR-211-5p and NUAK1 expression during the development of AD pathology, we examined their expression levels in the cortexes of APP/PS1 and WT mice with ages spanning from 2 to 18 months by real-time quantitative PCR using TaqMan probe. [score:6]
It was confirmed that overexpression of NUAK1 could rescue miR-211-5p mimic -induced neurite impairment (Figures 3E–H), indicating that miR-211-5p inhibits both neurite growth and branching by regulating NUAK1. [score:6]
MicroRNA-211 expression promotes colorectal cancer cell growth in vitro and in vivo by targeting tumor suppressor CHD5. [score:6]
MiR-211-5p expression is down-regulated during the embryonic development after E12.5 followed by an increase after birth (Figure 2A). [score:6]
To determine whether the effect of miR-211-5p is involved in Aβ1-42 impairment, we overexpressed miR-211-5p mimic or inhibitor in cultured cortical neurons followed by Aβ treatment. [score:5]
When Aβ was treated together with miR-211-5p overexpression, the cell death was further induced, but miR-211-5p inhibitor showed no effect (Figure 6B). [score:5]
The viability of primary cultured cortical neurons was dramatically decreased with the overexpression of miR-211-5p, whereas miR-211-5p inhibitor had no effect (Figure 6A). [score:5]
miR-211 suppresses epithelial ovarian cancer proliferation and cell-cycle progression by targeting Cyclin D1 and CDK6. [score:5]
In this study, we found that miR-211-5p regulated neurite outgrowth by targeting NUAK1. [score:4]
However, miR-211-5P inhibitor had no effect (Figure 1), indicating that additional unknown mechanisms may also be involved in NUAK1 regulation. [score:4]
To determine whether NUAK1 is regulated by miR-211-5p in Neuro2A cells and primary cultured cortical neurons, we transfected cells with miR-211-5p mimic and inhibitor and then examined the NUAK1 mRNA and protein levels. [score:4]
MiR-211-5p Inhibits Neurite Growth and Branching via Targeting NUAK1. [score:4]
Our previous study found that miR-211-5p was up-regulated in the cortexes of APPswe/PS1ΔE9 double transgenic mice, which are commonly used as an AD mouse mo del, suggesting the pivotal role of miR-211-5p in AD pathology (Luo et al., 2014). [score:4]
To gain insight into the role of miR-211-5p in neurogenesis, qPCR, and Western blotting were performed to assess the expression levels of miR-211-5p and NUAK1 during mouse embryonic and postnatal cortex development. [score:4]
FIGURE 2 Expression profile of miR-211-5p and NUAK1 in mice brains during development. [score:4]
FIGURE 3 MiR-211-5p inhibits neurite growth and branching via its target NUAK1. [score:4]
Over -expression of miR-211-5p mimic resulted in a significant decrease of NUAK1 mRNA and protein levels. [score:3]
The mimic and inhibitor of miR-211-5p and controls were purchased from Ribo Bio Company. [score:3]
The result showed that the longest neurite branching is still significantly reduced when miR-211-5p was overexpressed (Figure 3D). [score:3]
As NUAK1 is one of the targets of miR-211-5p, we further determined whether NUAK1 could alleviate the insult of miR-211-5p on neurite length and branching in cortical neurons. [score:3]
However, there are no relative reports about the role of miR-211 in neuronal differentiation and neurodegenerative diseases at present. [score:3]
FIGURE 4 Expression profile of miR-211-5p and NUAK1 in APP/PS1 mice cortexes and Aβ -treated primary cortical neurons. [score:3]
NUAK1 mRNA and protein are highly expressed from E12.5 to P0, which is in contrast to that of the miR-211-5p (Figures 2B,C). [score:3]
NUAK1 has been demonstrated to be one of the targets of miR-211-5p with three miR-211-5p binding sites in its 3′UTR (Bell et al., 2014). [score:3]
Transcription factor/microRNA axis blocks melanoma invasion program by miR-211 targeting NUAK1. [score:3]
However, there is no effect of miR-211-5p inhibitor on neuron viability, indicating that there are more factors involved in this complicated process, such as bcl-2 (An et al., 2014). [score:3]
However, miR-211-5p inhibitor protected neurons from Aβ damage (Figures 5E–H). [score:3]
Overexpression of miR-211-5p mimic dramatically aggravated the longest neurite length and branching damage induced by Aβ (Figures 5A–D). [score:3]
However, our study supports the translational potential of miR-211-5p in AD diagnosis and treatment in the future. [score:3]
FIGURE 1 MiR-211-5p regulates NUAK1 expression in Neuro-2a cells and primary mouse cortical neurons. [score:3]
In order to examine the role of miR-211-5p on neuron viability, an MTT assay was performed after miR-211-5p mimic or inhibitor transfection. [score:2]
Studies have shown that miR-211-5p regulates cell proliferation, differentiation, survival, invasion, and metastasis (Asuthkar et al., 2012; Cai et al., 2012; Bell et al., 2014; Xia et al., 2015). [score:2]
MiR-211-5p expression was significant higher in APP/PS1 mice than that of WT mice beginning at 9 months of age (Figure 4A). [score:2]
The dynamic changes of miR-211-5p and NUAK1 were consistent with that from mice tissues (Figures 4D,E), indicating that miR211-5p-regulated NUAK1 pathway may have a relationship with the pathological process of AD. [score:2]
For example, miR-211-5p knockout mice will be crossed with APP/PS1 mice to further confirm the role of miR-211-5p in Aβ -induced neurogenesis impairment. [score:2]
Epigenetic regulation of miRNA-211 by MMP-9 governs glioma cell apoptosis, chemosensitivity and radiosensitivity. [score:2]
MiR-211-5p expression was quantified by semi-quantitative RT-PCR with SYBR Green (D). [score:2]
MiR-211-5p was not only involved in neuronal differentiation at embryonic stage, but also involved in Aβ -induced pathologies in an AD mouse mo del by targeting NUAK1. [score:2]
MiR-211-5p-NUAK1 Pathway Is Involved in Alzheimer’s Disease Pathologies. [score:2]
Our work indicated that miR-211-5p may play a role in AD development by affecting neurogenesis and neuronal viability. [score:2]
Primer/probe name Sequence U6-F 5′-GCTTCGGCAGCACATATACTAAAAT-3′ U6-R 5′-CGCTTCACGAATTTGCGTGTCAT-3′ MiR-211-5p-F 5′-GATCTTCCCTTTGTCATCC-3′ Has miR-R 5′-GTGTCGTGGAGTCGGCAA-3′ MiR-211-5p-RT 5′-GTCGTATCCAGTGCGTGTCGTGGAGTCGGCAATTGCACTGGATACGACAGGCAA-3′ MsGAPDH-F 5′-AACTTTGGCATTGTGGAAGG-3′ MsGAPDH-R 5′-GGATGCAGGGATGATGTTCT-3′ MsNUAK1-F 5′-GAGCCCACTCTATGCGTC-3′ MsNUAK1-R 5′-ATGTCCTCGATGGTGGCT-3′ MiR-211-5p probe 5′-FAM-CACTGGATACGACAGGCAAAGGAT-TAMRA-3′ U6 probe 5′-FAM-CCTTGCGCAGGGGCCATGCTAATC-TAMRA-3′ Mouse cortical tissues or cultured cells were lysed in RIPA buffer [150 mM NaCl, 1% (v/v) Nonidet P-40, 0.5% deoxycholic acid, 0.1% (w/v) sodium dodecyl sulfate (SDS)] containing protease inhibitors (cocktail, Sangon) and 1 mM phenylmethanesulfonyl fluoride (Sigma) for 15 min. [score:2]
FIGURE 5 miR-211-5p aggravates the insult of Aβ on neurite growth and branching. [score:1]
The mechanism of miR-211-5p increase induced by Aβ is still unknown, but our data shows that the destructive role of miR-211-5p on neurogenesis participates in the Aβ impairment of neurons. [score:1]
We still need more animal experiments to confirm the role of miR-211-5p further in AD. [score:1]
As miRNAs play roles as a network during different processes, the importance of miR-211-5p in Aβ-related pathologies still needs detailed elucidation. [score:1]
FIGURE 6 miR-211-5p increases Aβ cytotoxicity on neuron viability. [score:1]
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6
[+] score: 154
In the adult eye, miR-211 is expressed in the RPE and in the Inner Nuclear Layer (INL) with a weaker expression detected in the Outer Nuclear Layer (ONL) and in the Ganglion Cell Layer (GCL) as previously reported [26] (Supplementary Fig.   2c,d), again recapitulating the expression pattern of its host gene [27]. [score:7]
Of these, the expression levels of 61 genes were significantly decreased upon miR-211 deletion, while only 2 genes were upregulated (listed in Supplementary Table  1). [score:6]
The cone loss observed in miR-211−/− mice could be a consequence of increased cell death, as also suggested by previous studies that have shown that miR-211 can directly regulate these events by modulating Chop expression [55]. [score:5]
First, RNA ISH expression data indicate that miR-211 is highly expressed in the RPE, INL and in the GCL (Supplementary Fig.   2c). [score:5]
Interestingly, we found that miR-211 is expressed in the RPE, INL, GCL and at lower levels in photoreceptor cells in the adult retina, recapitulating in full the expression pattern of its host gene previously reported in the human retina [27]. [score:5]
By RNA in situ hybridization (ISH), we showed that the expression of miR-211 is abundant in the developing eye and is detected in the presumptive RPE, ciliary body, distal region of the developing retina of the optic cup thus recapitulating the expression of its host gene, the melastatin, transient receptor potential cation channel subfamily M member 1 (Trpm1) gene (Supplementary Fig.   1). [score:5]
Therefore, we asked whether the deletion of pre-miR-211 could have any effect on the proper expression of Trpm1, which could contribute to the phenotype of miR-211−/− mice. [score:3]
Differentially expressed genes between conditions (miR-211−/− vs WT) were detected using the Generalized Linear Mo del approach implemented in the Bioconductor package “edgeR” [74]. [score:3]
Figure 1One month old miR-211−/− mice display a normal expression pattern of photoreceptor markers but initial signs of cone dysfunction. [score:3]
Preliminary data suggest that miR-211 expression is controlled by the transcription factor MITF and that this miRNA could contribute to RPE differentiation [24]. [score:3]
Next we performed differential gene expression analysis to determine the transcriptional effects of miR-211 deletion. [score:3]
Moreover, we also detect additional metabolic pathways such as pyruvate and lipid metabolic processes, suggesting that miR-211 might function as a metabolic switch factor controlling the homeostasis of miR-211 -expressing cells. [score:3]
However, recent findings also highlighted a distinct and context -dependent targeting activities exerted by the miR-204 and miR-211 paralogs [54]. [score:3]
MiR-211 is one of the most abundant miRNAs in the retina [25] and its expression is sensitive to light levels [26]. [score:3]
The latter miRNA, since it shares with miR-211 the same seed region, and therefore is predicted to target a similar set of genes, can in principle compensate at least in part the lack of miR-211. [score:3]
Remarkably, the RBCs from miR-211−/− mice did not show any significant alteration from the behaviour of age matched controls in terms of light sensitivity, photovoltage amplitude and ion channel expression (Fig.   3e–h). [score:3]
Second, miR-211 seems to be co-expressed with the Trpm1 gene, which is known to play a relevant role in bipolar cell functionality 34– 36. [score:3]
Concordantly, by RNA ISH we detected no miR-211 expression in the retina of miR-211−/− mice at P30 (Supplementary Fig.   2c–e). [score:3]
Western blot analysis showed no altered expression of any of the Trpm1 isoforms upon miR-211 deletion in the retina (Supplementary Fig.   3a,b). [score:3]
In miR-211−/− retinas the pattern of expression of the bipolar cell markers analysed is similar to wt mice. [score:3]
Interestingly, previous studies have shown that alteration of miR-211 expression was associated with increase of vascular invasion in cancer [44]. [score:3]
Although the effects of miR-211 inactivation seem to be mostly restricted to cone photoreceptor cells, yet this miRNA does not seem to display high levels of expression in this cell type. [score:3]
This is the first study to reveal the direct involvement of miR-211 in the visual system, extending the functional role of this miRNA family to cone photoreceptors. [score:2]
Indeed, an abnormal regulation of energy metabolism has been recently reported for miR-211 in human melanoma cells [57]. [score:2]
In summary, we have begun to dissect the function of miR-211 in eye development and function by demonstrating that it plays an important role in cone photoreceptor maintenance and function. [score:2]
MiR-211 coordinates expression of genes relevant to retinal metabolism. [score:2]
Analysis of the expression of the Chx10 (bipolar), PKC-α (rod bipolar), GS (Müller), Pax6 (amacrine and ganglion cells) and Calbindin (horizontal) markers, did not reveal any significant defects in other adult retinal cell types in miR-211−/− mice (7 months old) when compared with age-matched controls (Fig.   3a–d and Supplementary Fig.   8). [score:2]
Generation of miR-211 knockout mice. [score:2]
The miR-211 knockout mouse line (mmu-mir-211−/−) employed in this study was generated by the Wellcome Trust Sanger Institute [28]. [score:2]
These observations together with the qRT-PCR analysis (Supplementary Fig.   3c) demonstrated that in miR-211−/− eyes, the expression levels of Trpm1 was not altered when compared with WT animals. [score:2]
Despite the pervasive role of miR-204 in many aspects of eye development and function, to date, there is very limited information on the function in the eye of its closely related paralog miR-211. [score:2]
As previously stated, miR-211 is an intragenic miRNA, which is located in an intronic region, i. e., between exon 6 and exon 7, of the Trpm1 gene [29]. [score:1]
MiR-211 first appeared in mammals through the evolution of one of the two copies of miR-204, which is present in two identical copies in the genomes of early vertebrates and fish, including Medaka fish 16, 17. [score:1]
To date, however, miR-211 function in the eye has not been thoroughly analysed and its in vivo role remains unclear. [score:1]
Overall, the above data suggest the presence of signs of cone dysfunction in 1-month old miR-211−/− mice in spite of apparently normal photoreceptor morphology. [score:1]
Altogether, these data suggest a relevant and specific role of miR-211 in the control of cone photoreceptor survival and function. [score:1]
616391-360 miR-211 and 699004-360, Exiqon,) were hybridized to frozen sections as described previously [66]. [score:1]
Proteins were extracted from eyes of wild type and miR-211−/− mice by homogenization in RIPA buffer. [score:1]
The amplitudes of the dark-adapted, scotopic a-wave and b-wave of the miR-211−/− mice are similar to the amplitudes of the wt control mice. [score:1]
Therefore, our data suggest that the ablation of miR-211 leads to a metabolic status change of retinal cells that may contribute to the cone dystrophy observed in miR-211−/− mice. [score:1]
To gain insight into the molecular basis underlying the miR-211 -induced phenotype, we decided to carry out transcriptome analysis of miR-211−/− mice by RNAseq. [score:1]
The b-wave amplitude of miR-211−/− mice is significantly lower than in wt mice in the light intensity ranges that stimulate only cone and rod-cone responses. [score:1]
As previously mentioned, the alterations of the mesopic response detected by ERG analysis in miR-211−/− mice (Figs  1 and 2, Supplementary Fig.   6) do not rule out some rod involvement. [score:1]
In mammals, miR-204 has a closely related paralog, miR-211 by which it only differs by one or two nucleotides in the mature sequence, depending on the species [17]. [score:1]
RNA-Seq libraries were prepared for each RNA sample in biological replicates, six WT and six miR-211−/− RNA samples, according to manufacturer’s instructions (TruSeq RNA Sample Preparation kit), with an initial amount of 4 μg of total RNA. [score:1]
Consistent with a progressive and ultimately severe functional cone deficiency observed from the age of 3-months onward, miR-211−/− mice showed a gradual reduction of cone density at these same stages (Fig.   2i and Supplementary Fig.   4a–e). [score:1]
We found that the mature miR-211 was not detectable in the retinas of all miR-211−/− mice that we examined (n = 3) (Supplementary Fig.   2b). [score:1]
Here, we establish, for the first time, the existence of a specific relationship between miR-211 activity and cone function and survival in mammals. [score:1]
From three months of age onward, there are significant differences in the number of cones between wt and miR-211−/− mice up to a greater than 50% reduction in aged miR-211−/− mice. [score:1]
However, a slight remo delling of aberrant processes of the PKC-α-bipolar positive cells was observed to extend through the ONL of the retina of miR-211−/− (Fig.   3), as a consequence of cone dystrophy 40, 41. [score:1]
miR-211 KO males. [score:1]
Notably, comparison of the morphology of the differentiated RPE/retina of control and miR-211−/− mice did not reveal significant alteration in thickness and laminar organization (Supplementary Fig.   9k–l). [score:1]
We also were not able to detect any TUNEL -positive cells in the retina of miR-211−/− mice (Supplementary Fig.   7a–l), reflecting a very slow degeneration of cones, which are not highly abundant in the mouse retina. [score:1]
However, miR-211 activity might be MAFA-independent, because no alteration of the MafA mRNA was observed in the miR-211−/− transcriptome. [score:1]
MiR-211−/− mice display a progressive cone dystrophyTo explore the phenotypic consequences of miR-211 deletion, we carried out a detailed analysis of miR-211 homozygous mutant mice. [score:1]
Overall, these data indicate that miR-211 deletion in mice leads to a progressive cone dystrophy phenotype. [score:1]
For wild type and miR-211−/− mice analysis, the RNAs were extracted from whole eyes. [score:1]
To increase the likelihood of detecting the transcriptome changes related to the functional phenotype and not those secondary to cone cell death, RNA-Seq libraries were prepared from whole eye, after removal of the lens and cornea from 1–2 month old miR-211−/− mice, stages in which cone cell loss was not yet detected. [score:1]
MiR-211 ablation leads to a specific cone dysfunctionTwo observations suggest that miR-211 could have additional functions in other retinal cell types, apart from cone photoreceptors. [score:1]
Two groups of six mice for both miR-211−/− and miR-211+/+ genotypes, were analysed for each time point. [score:1]
Here, by analysing the functional consequences of miR-211 loss-of-function in mice, we show that this miRNA is essential for cone photoreceptor maintenance and function. [score:1]
The strain was obtained by deleting 160 bp (containing the pre-miR-211) from the wild type sequence. [score:1]
Supplementary Data Supplementary Table 1 Supplementary Table 2 We are grateful to F. Giuseppe Salierno and Edoardo Nusco for technical support, Alison Forrester for critical reading of the manuscript and Allan Bradley for providing the miR-211−/− mouse. [score:1]
To explore miR-211 function in vivo, we generated a miR-211 -deficient mouse line in which the precursor sequence of miR-211 (pre-miR-211) was deleted by homologous recombination [28] (Supplementary Fig.   2a). [score:1]
Two observations suggest that miR-211 could have additional functions in other retinal cell types, apart from cone photoreceptors. [score:1]
H. P. provided miR-211−/− mice and analysed the data. [score:1]
The possibility of a miR-211 -mediated control of retinal metabolism is particularly attractive; indeed, previous reports have proposed that the paralog miR-204 is able to block insulin production during the diabetic process [56], in which a progressive retinopathy is frequently associated as secondary pathological hallmark. [score:1]
The latter result may be explained by both the slow rate of cone degeneration observed in miR-211−/− mice and by the low abundance of cones, which represent the 3% of photoreceptor cells in the retina that can preclude the detection of cone cell death. [score:1]
Overall, the mode of action of miR-211 and its relevance in the control of retinal metabolism and catabolism processes as well as in the function of other retinal cell types (e. g., bipolar cells in which miR-211 is particularly abundant) might be more complex and require further study. [score:1]
Therefore, we asked whether the retinal vasculature was impaired in miR-211−/− mice. [score:1]
RNA-Seq libraries were prepared for each eye sample in multiple biological replicates, five for WT and six for miR-211−/− animals. [score:1]
Thus, we then examined whether cones and rods degenerate in miR-211−/− mice at P30. [score:1]
Characterization of miR-211−/− mice MiR-211 is one of the most abundant miRNAs in the retina [25] and its expression is sensitive to light levels [26]. [score:1]
Crucially, these changes were not associated with defects in rod density or a significant reduction in ONL thickness (Supplementary Fig.   4f,g), further supporting the observation that miR-211 depletion induces a cone-specific dystrophy. [score:1]
To explore the phenotypic consequences of miR-211 deletion, we carried out a detailed analysis of miR-211 homozygous mutant mice. [score:1]
Moreover, we detected no alteration in Trpm1 mRNA maturation and splicing by both RT-PCR (Supplementary Fig.   3d) and qRT-PCR analyses (Supplementary Fig.   3e) further confirming the specificity of miR-211 depletion. [score:1]
In all experiments, we used as controls aged-matched littermates of miR-211−/− mice. [score:1]
However, we cannot exclude that cone dysfunction in miR-211−/− mice might at least in part be also due to non-cell autonomous effects. [score:1]
Representative immunofluorescence images of wild type (a,c) and miR-211−/− (b,d) mouse retinas at 7 months, stained with anti-Chx10 (a,b) and anti-PKC-alpha (c,d) antibodies. [score:1]
In particular, we included in the study two males and three females with a miR-211+/+ genotype, and six males with a miR-211−/− genotype. [score:1]
flash strength from control (black circles; n = 6) and miR-211−/− RBCs (white circles; n = 6). [score:1]
In particular, we found that miR-211 inactivation in mouse leads to a progressive cone dysfunction followed by cone loss, without the apparent involvement of rods. [score:1]
Interestingly, our transcriptome analysis suggests that miR-211 could be involved in controlling the metabolism and catabolism of retinal cells, including genes participating in glucose, pyruvate and lipid metabolic process. [score:1]
The amplitudes of the dark-adapted, scotopic a-wave and b-wave of miR-211−/− mice are significantly lower at higher intensities than in wt control mice. [score:1]
However, a slight remo delling of aberrant processes of the PKC-α-bipolar positive cells was observed to extend through the ONL of the retina of miR-211−/− (magnified in white boxes). [score:1]
In most mammals, including mouse, miR-211 only shows one nucleotide difference with the mature sequence of miR-204. [score:1]
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7
[+] score: 74
Our data demonstrate that overexpression of β-catenin activates miR-211, and that activation of Wnt/β-catenin signalling by BIO and CHIR upregulates miR-211 expression. [score:8]
The sequencing data shows that miR-211 is dramatically upregulated in response to BIO and CHIR treatment (Supplementary Data 3 and 4) even though most other miRNAs are downregulated. [score:7]
These data reveal that β-catenin increases the expression of miR-211 and that activation of Wnt/β-catenin signalling by GSK3 inhibitors induces miR-211 expression. [score:7]
qPCR results showed that overexpression of β-catenin significantly upregulates pri-miR-211 and miR-211-3p in J1 mESCs (Fig. 5e). [score:6]
Since BIO and CHIR are able to activate Wnt/β-catenin signalling by stabilising β-catenin, we wanted to determine if either BIO- or CHIR -upregulated miR-211 is mediated directly by β-catenin. [score:5]
The expression of primary and mature miR-211 in β-catenin overexpressed J1 mESCs was determined by qPCR. [score:5]
GSK3 inhibitors and β-catenin induce the expression of miR-211. [score:5]
The qPCR results further confirmed that both Trpm1 and pri-miR-211 were upregulated following either BIO or CHIR treatment (Fig. 5a and b). [score:4]
The expression of primary and mature miR-211 in β-catenin knockdown J1 mESCs was determined by qPCR. [score:4]
Consistently, the mature form of miR-211 was significantly upregulated by BIO and CHIR treatment (Fig. 5c). [score:4]
Mouse miR-211 is located on chromosome 7 and embedded in intron 2 of the transient receptor potential cation channel subfamily member 1 (Trpm1) gene, indicating that miR-211 might be expressed similarly to Trpm1. [score:3]
Activation of Wnt/β-catenin signalling induces miR-211 expression in mESCs. [score:3]
Furthermore, the results demonstrate that activation of Wnt/β-catenin signalling by BIO or CHIR induces miR-211 expression. [score:3]
It should be noted that miR-211 was strongly increased in both BIO- and CHIR -treated J1 mESCs, and that miR-181a was inhibited by both BIO and CHIR (Fig. 3i, 3j). [score:3]
Therefore, we analysed the expression of both primary and mature forms of miR-211 under varying levels of β-catenin. [score:3]
Furthermore, knockdown of β-catenin led to a reduction of both primary and mature miR-211 (Fig. 5f). [score:2]
Full-length blots are presented in Supplementary Figure 7. J1 mESCs were treated with 1 μM BIO, 3 μM CHIR or equal volume of DMSO (control) for 24 h, the transcription levels of Trpm1 (a), pri-miR-211 (b) and mature form miR-211 (c) were determined by qPCR. [score:1]
Further investigation is needed to identify miR-211 target genes and their function in ESCs. [score:1]
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8
[+] score: 31
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-29a, hsa-mir-33a, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-107, hsa-mir-16-2, mmu-let-7g, mmu-let-7i, mmu-mir-1a-1, mmu-mir-29b-1, mmu-mir-124-3, mmu-mir-126a, mmu-mir-9-2, mmu-mir-132, mmu-mir-133a-1, mmu-mir-134, mmu-mir-138-2, mmu-mir-145a, mmu-mir-152, mmu-mir-10b, mmu-mir-181a-2, hsa-mir-192, mmu-mir-204, mmu-mir-206, hsa-mir-148a, mmu-mir-143, hsa-mir-7-1, hsa-mir-7-2, hsa-mir-7-3, hsa-mir-10b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-204, hsa-mir-211, hsa-mir-212, hsa-mir-181a-1, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, mmu-mir-106b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-143, hsa-mir-145, hsa-mir-152, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-134, hsa-mir-138-1, hsa-mir-206, mmu-mir-148a, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-15a, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-18a, mmu-mir-20a, mmu-mir-21a, mmu-mir-29a, mmu-mir-29c, mmu-mir-34a, mmu-mir-330, hsa-mir-1-1, mmu-mir-1a-2, hsa-mir-181b-2, mmu-mir-107, mmu-mir-17, mmu-mir-212, mmu-mir-181a-1, mmu-mir-33, mmu-mir-29b-2, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, mmu-mir-181b-1, mmu-mir-7a-1, mmu-mir-7a-2, mmu-mir-7b, hsa-mir-106b, hsa-mir-29c, hsa-mir-34b, hsa-mir-34c, hsa-mir-330, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-181b-2, hsa-mir-181d, hsa-mir-505, hsa-mir-590, hsa-mir-33b, hsa-mir-454, mmu-mir-505, mmu-mir-181d, mmu-mir-590, mmu-mir-1b, mmu-mir-145b, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, mmu-mir-126b, mmu-mir-9b-2, mmu-mir-124b, mmu-mir-9b-1, mmu-mir-9b-3
MiR-211 expression promotes colorectal cancer growth by down -regulating expression of the CHD5 tumor suppressor (Cai et al., 2010). [score:7]
MicroRNA-211 expression promotes colorectal cancer cell growth in vitro and in vivo by targeting tumor suppressor CHD5. [score:6]
Increased miR-211 expression is linked with progression and vascular invasion of oral carcinoma (Chang et al., 2008). [score:3]
Intronic miR-211 assumes the tumor suppressive function of its host gene in melanoma. [score:3]
Association between high miR-211 microRNA expression and the poor prognosis of oral carcinoma. [score:3]
miRNA Gene targets miR-134Brain-derived neurotrophic factor (BDNF) and cAMP response element -binding factor (CREB) miR-204 BDNF and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) miR-211 BDNF and AMPA miR-505 BDNF and AMPA miR-590-3p BDNF and CREB MiR-134 has an important role in the brain, where it is essential for activity -dependent dendritic outgrowth, nerve growth cone guidance, and size of dendritic spines of hippocampal neurons (Schratt et al., 2006; Khudayberdiev et al., 2009; Han et al., 2011). [score:3]
miRNA Gene targets miR-134Brain-derived neurotrophic factor (BDNF) and cAMP response element -binding factor (CREB) miR-204 BDNF and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) miR-211 BDNF and AMPA miR-505 BDNF and AMPA miR-590-3p BDNF and CREBMiR-134 has an important role in the brain, where it is essential for activity -dependent dendritic outgrowth, nerve growth cone guidance, and size of dendritic spines of hippocampal neurons (Schratt et al., 2006; Khudayberdiev et al., 2009; Han et al., 2011). [score:3]
MiR-211 is also implicated as a tumor suppressor for melanoma invasion (Levy et al., 2010). [score:2]
MiR-211 has a binding site for angiopoietin-1, which is a vascular strengthening factor during vascular development and a protective factor for pathological vascular inflammation and leakage, including brain vascular leakage as occurs in stroke (Chen et al., 2010). [score:1]
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9
[+] score: 26
Other miRNAs from this paper: mmu-mir-204, mmu-mir-34a
Although the functional significance and targets of miR-204 upregulation in fibroblasts was not explored, miR-211 downregulated the ER stress protein CHOP by an unusual mechanism involving transcriptional repression of the CHOP promoter, thereby functioning as a pro-survival microRNA during ER stress. [score:9]
Chitnis NS miR-211 is a prosurvival microRNA that regulates chop expression in a PERK -dependent mannerMol Cell. [score:4]
However, it is worth noting that thapsigargin -induced upregulation of miR-211, a closely related microRNA which differs from miR-204 by only one nucleotide but shares the same seed sequence (UUUCCCU), in mouse embryonic fibroblasts is dependent on PERK [32]. [score:4]
Chitnis NS miR-211 is a prosurvival microRNA that regulates chop expression in a PERK -dependent mannerMolecular cell. [score:4]
Furthermore, both miR-204 and miR-211, which is encoded in the TRPM1 gene and transcribed independently from miR-204, are upregulated with thapsigargin and low glucose-stimulated ER stress in mouse embryonic fibroblasts [34]. [score:4]
Additionally, miR-211, which shares an almost identical sequence with miR-204, is induced in a PERK -dependent manner [11]. [score:1]
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10
[+] score: 25
The median log expression of the ten most deregulated miRNAs is given in Figure 4. The most up-regulated miRNA, mmu-mir-205-5p, was 135 times higher and the most down-regulated miRNA, mmu-mir-211-5p, was 35.7 times lower expressed in the curcumin -treated samples (Table 1). [score:12]
The ten most up-regulated miRNAs included mmu-miR-205-5p, mmu-miR-222-3p, mmu-miR-205-3p, mmu-miR-146b-5p, mmu-miR-21-5p, mmu-miR-21-3p, mmu-miR-221-3p, mmu-miR-140-3p, mmu-miR-142-5p, and mmu-miR-140-5p and the ten most down-regulated miRNAs comprised mmu-miR-211-5p, mmu-miR-3096-5p, mmu-miR-711, mmu-miR-466h-5p, mmu-miR-130b-3p, mmu-miR-3082-5p, mmu-miR-1199-5p, mmu-miR-669b-5p, mmu-miR-1187, and mmu-miR-1224-5p (Table 1). [score:7]
For example, down-regulation of hsa-miR-211-5p has been shown to be associated with melanoma progression [38], [46] and not as observed in the present study with inhibition of tumor growth in curcumin -treated melanoma. [score:6]
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11
[+] score: 16
Lack of MITF expression presumably results in high BRN2 levels, given that MITF represses BRN2 via miR-211 expression [16], and BRN2 binds the MITF promoter to directly repress its expression in vitro [8]. [score:8]
In addition, expression of miR-211, a target of MITF, either increased or decreased BRN2 levels and invasive capacity depending on the cell line and constitutive level of MITF present [16]. [score:5]
We have additionally shown a role for MITF in reducing BRN2 protein levels by controlling expression of miR-211, highlighting a feedback loop for the levels of these transcription factors [16]. [score:3]
[1 to 20 of 3 sentences]
12
[+] score: 12
As compared with cells under normxia, miR-711, miR-714, miR-328, miR-346, miR-210, miR-744, miR-5130, miR-181a and miR-2137 were significantly over-expressed in hypoxia/reperfusion treated cardiomyocytes, while the expression of miR-491, miR-211, miR-532, miR-185, miR-425, miR-128, miR-24 was down-regulated (Figure 4B). [score:7]
As expected, miR-2137, miR-210, miR-5130, and miR-328 were highly expressed in cardiomyocytes, while miR-490, miR-491, and miR-211 were expressed at a low level. [score:5]
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13
[+] score: 10
In HepG2 cells, miR-192, miR-204, miR-18, miR-19 and miR-211 could down-regulate HOTTIP expression (all P<0.05). [score:6]
All miRNA mimics (miR-138, miR-18, miR-192, miR-215, miR-19, miR-204 and miR-211), miRNA inhibitors(miR-192 and miR-204) and small interfering RNA (siRNA) duplexes (siHOTTIP-1 and siHOTTIP-2) were products of Genepharma (Shanghai, China). [score:3]
20 nmol/L mimics of miR-138, miR-18, miR-192, miR-215, miR-19, miR-204, and miR-211, two HOTTIP siRNAs (siHOTTIP-1 and siHOTTIP-2)or NC RNA were transfected into SMMC7721,HepG2 and Hep3B HCC cells. [score:1]
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14
[+] score: 9
1 regulates CD44 as a molecular decoy for miR211-3p 26974151 miR-32-3p −54 Acts a a tumor suppressor in NSCLC 26229485 miR-3082-5p −55 Unknown miR-3960 −56 miR-3960 regulated cellular growth and proliferation through a regulatory feedback loop with miR-2861, respnse to oxidative stress 21324897, 26539117 miR-466i-5p −49 Unknown miR-468-3p −57 Unknown miR-574-5p −53 Oncogene in various cancer types, incl. [score:6]
Nd11 Function PMID miR-188-5p −65 Acts as a tumor suppressor in prostate caner 25714029 miR-1187 −54 Involved in hepatocyte apoptosis 22266786 miR-1196-5p −37 Unknown miR-211-3p −55 lncRNA-uc002kmd. [score:3]
[1 to 20 of 2 sentences]
15
[+] score: 9
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-19a, hsa-mir-19b-1, hsa-mir-19b-2, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-31, hsa-mir-100, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-16-2, mmu-mir-23b, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-127, mmu-mir-128-1, mmu-mir-132, mmu-mir-133a-1, mmu-mir-188, mmu-mir-194-1, mmu-mir-195a, mmu-mir-199a-1, hsa-mir-199a-1, mmu-mir-200b, mmu-mir-205, mmu-mir-206, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-122, mmu-mir-30e, hsa-mir-199a-2, hsa-mir-199b, hsa-mir-205, hsa-mir-211, hsa-mir-212, hsa-mir-214, hsa-mir-217, hsa-mir-200b, hsa-mir-23b, hsa-mir-27b, hsa-mir-30b, hsa-mir-122, hsa-mir-128-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-127, hsa-mir-138-1, hsa-mir-188, hsa-mir-194-1, hsa-mir-195, hsa-mir-206, mmu-mir-19b-2, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-16-1, mmu-mir-16-2, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-31, mmu-mir-351, hsa-mir-200c, mmu-mir-17, mmu-mir-19a, mmu-mir-100, mmu-mir-200c, mmu-mir-212, mmu-mir-214, mmu-mir-26a-2, mmu-mir-29b-2, mmu-mir-199a-2, mmu-mir-199b, mmu-mir-19b-1, mmu-mir-138-1, mmu-mir-128-2, hsa-mir-128-2, mmu-mir-217, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, mmu-mir-412, mmu-mir-431, hsa-mir-431, hsa-mir-451a, mmu-mir-451a, mmu-mir-467a-1, hsa-mir-412, hsa-mir-485, hsa-mir-487a, hsa-mir-491, hsa-mir-503, hsa-mir-504, mmu-mir-485, hsa-mir-487b, mmu-mir-487b, mmu-mir-503, hsa-mir-556, hsa-mir-584, mmu-mir-665, mmu-mir-669a-1, mmu-mir-674, mmu-mir-690, mmu-mir-669a-2, mmu-mir-669a-3, mmu-mir-669c, mmu-mir-696, mmu-mir-491, mmu-mir-504, hsa-mir-665, mmu-mir-467e, mmu-mir-669k, mmu-mir-669f, hsa-mir-664a, mmu-mir-1896, mmu-mir-1894, mmu-mir-1943, mmu-mir-1983, mmu-mir-1839, mmu-mir-3064, mmu-mir-3072, mmu-mir-467a-2, mmu-mir-669a-4, mmu-mir-669a-5, mmu-mir-467a-3, mmu-mir-669a-6, mmu-mir-467a-4, mmu-mir-669a-7, mmu-mir-467a-5, mmu-mir-467a-6, mmu-mir-669a-8, mmu-mir-669a-9, mmu-mir-467a-7, mmu-mir-467a-8, mmu-mir-669a-10, mmu-mir-467a-9, mmu-mir-669a-11, mmu-mir-467a-10, mmu-mir-669a-12, mmu-mir-3473a, hsa-mir-23c, hsa-mir-4436a, hsa-mir-4454, mmu-mir-3473b, hsa-mir-4681, hsa-mir-3064, hsa-mir-4436b-1, hsa-mir-4790, hsa-mir-4804, hsa-mir-548ap, mmu-mir-3473c, mmu-mir-5110, mmu-mir-3473d, mmu-mir-5128, hsa-mir-4436b-2, mmu-mir-195b, mmu-mir-133c, mmu-mir-30f, mmu-mir-3473e, hsa-mir-6825, hsa-mir-6888, mmu-mir-6967-1, mmu-mir-3473f, mmu-mir-3473g, mmu-mir-6967-2, mmu-mir-3473h
Out of these 25 miRNAs, 18 miRNAs were differentially expressed in a consistent manner between the 2 groups (Figure 4A, highlighted); 8 miRNAs were downregulated in both groups (miR-16, miR-200, miR-205, miR-3064, miR-379, miR-431, miR-485 and miR-491) and 10 miRNAs were upregulated in both groups (miR-194, miR-1894, miR-211, miR-3072, miR- 3077, miR-4436, miR-5128, miR-669a, miR-669c and miR-6967). [score:9]
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[+] score: 9
Although miR-204 is expressed in MG, RPE cells and ciliary epithelial cells, it is unlikely that the MG in our study was contaminated by RPE or ciliary epithelial cells, since (1) the FACS-sorted tdTomato [+] cells in our samples were Sox2 [+] and this is not expressed in either the RPE or ciliary epithelium and (2) miRNAs miR-211, miR-222, and miR-221, are highly expressed in the RPE 39, but were not highly expressed in the MG-fraction in our study. [score:9]
[1 to 20 of 1 sentences]
17
[+] score: 9
The miRNA with the least dysregulated targets was hsa-miR-211 (52 targets) while hsa-miR-23b was the miRNA with the most dysregulated targets (115). [score:9]
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[+] score: 8
Other miRNAs from this paper: mmu-mir-331
Manipulating GAPLINC expression altered CD44 mRNA abundance and regulated cell migration and proliferation by suppressing CD44 expression as a molecular decoy for miR211-3p [24]. [score:8]
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19
[+] score: 8
We initially focused on promoter hypermethylation to explain downregulation of this gene in our sample series of T-LBL, but despite a substantial reduction in the levels of mRNA in almost all samples in the exploratory cohort (7/8), only two samples (840 and 521) (2/8) exhibited significant hypermethylation density (Fig. 4), and six out of eight (including tumor 840 with promoter hypermethylation) exhibited upregulation of one or two miRNAs selected for CDKN1C regulation (miR-211–3p and miR-222-3p). [score:8]
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[+] score: 7
Relative luciferase activity in NRCMs harbouring the reporter and transfected with control pcDNA3.1 vector or miR-221, miR-222, miR-211, miR-204 or miR-135a expression vectors. [score:3]
Deletion of the miR-221/222 binding site in the Angptl2-3′UTR reporter (Fluc-Angptl2-3'UTR-Δ 221/222) was performed using a PrimeSTAR mutagenesis basal kit (Takara Bio) according to the manufacturer's instructions miR-221, miR-222, miR-211, miR-204 or miR-135a overexpression vectors were constructed by inserting sequences including the full-length mature microRNA sequences into pBApo-CMV (Takara Bio). [score:3]
org database identified five candidates, including miR-135a, miR-204, miR-211, miR-221 and miR-222, predicted to bind to the Angptl2 mRNA 3′UTR. [score:1]
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[+] score: 7
The upregulated miRNAs included mmu-miR-34a-5p, mmu-miR-129b-5p, mmu-miR-451a, mmu-miR-144-5p and mmu-miR-129b-3p, whereas highly downregulated miRNAs included mmu-miR-100-5p, mmu-miR-99a-5p, mmu-miR-33-5p, mmu-miR-125a-5p, mmu-miR-128-1-5p, mmu-miR-181b-1-3p, mmu-miR-188-5p, mmu-miR-196b-5p, mmu-miR-211-5p, mmu-miR-224-5p, mmu-miR-455-3p, mmu-miR-504-5p, mmu-miR-592-5p, mmu-miR-5107-3p, mmu-miR-5120, and mmu-let-7i-3p. [score:7]
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22
[+] score: 6
The suppression of miR-155 was also discovered the study of the influence of several isoflavones from soy on prostate cancer cell lines, where miR-155, miR-208b, miR-211, miR-376a and miR-411 were found to be downregulated by the isoflavones by more than three to five fold than control cells [32]. [score:6]
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23
[+] score: 5
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-15a, hsa-mir-18a, hsa-mir-33a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-mir-27b, mmu-mir-126a, mmu-mir-128-1, mmu-mir-140, mmu-mir-146a, mmu-mir-152, mmu-mir-155, mmu-mir-191, hsa-mir-10a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, mmu-mir-297a-1, mmu-mir-297a-2, hsa-mir-27b, hsa-mir-128-1, hsa-mir-140, hsa-mir-152, hsa-mir-191, hsa-mir-126, hsa-mir-146a, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-15a, mmu-mir-18a, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-342, hsa-mir-155, mmu-mir-107, mmu-mir-10a, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, hsa-mir-374a, hsa-mir-342, gga-mir-33-1, gga-let-7a-3, gga-mir-155, gga-mir-18a, gga-mir-15a, gga-mir-218-1, gga-mir-103-2, gga-mir-107, gga-mir-128-1, gga-mir-140, gga-let-7a-1, gga-mir-146a, gga-mir-103-1, gga-mir-218-2, gga-mir-126, gga-let-7a-2, gga-mir-27b, mmu-mir-466a, mmu-mir-467a-1, hsa-mir-499a, hsa-mir-545, hsa-mir-593, hsa-mir-600, hsa-mir-33b, gga-mir-499, gga-mir-211, gga-mir-466, mmu-mir-675, mmu-mir-677, mmu-mir-467b, mmu-mir-297b, mmu-mir-499, mmu-mir-717, hsa-mir-675, mmu-mir-297a-3, mmu-mir-297a-4, mmu-mir-297c, 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-466d, hsa-mir-297, mmu-mir-467e, mmu-mir-466l, mmu-mir-466i, mmu-mir-466f-4, mmu-mir-466k, mmu-mir-467f, mmu-mir-466j, mmu-mir-467g, mmu-mir-467h, hsa-mir-664a, hsa-mir-1306, hsa-mir-1307, gga-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, gga-mir-10a, mmu-mir-1306, mmu-mir-3064, 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-466, hsa-mir-3173, hsa-mir-3618, hsa-mir-3064, hsa-mir-499b, mmu-mir-466q, hsa-mir-664b, gga-mir-3064, mmu-mir-126b, gga-mir-33-2, mmu-mir-3618, mmu-mir-466c-3, gga-mir-191
Out of the 26 miRNA/host gene pairs with coordinated expression, 11 have been found to be coordinately expressed in both, human and mouse [19], [27], [59], [61]– [64], [67]– [69], [71], [73]– [79]: mir-103/ PANK3, mir-107/ PANK1, mir-126/ EGFL7, mir-128-1/ R3HDM1, mir-140/ WWP2, mir-211/ TRPM1, mir-218-1/ SLIT2, mir-218-2/ SLIT3, mir-27b/ C9orf3, mir-33/ SREBF2, and mir-499/ MYH7B. [score:5]
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24
[+] score: 5
Other miRNAs from this paper: mmu-mir-204, ola-mir-204
miR-204 in ocular physiology and developmentIn mammals, miR-204 has a closely related paralog the miR-211. [score:2]
In mammals, miR-204 has a closely related paralog the miR-211. [score:1]
Interestingly, miR-211 first appears in mammals through the evolution of one of the two copies of miR-204, which is present in two identical copies in the genomes of early vertebrates and fish, including medaka fish [17]. [score:1]
miR-204 and miR-211 differ by one or two nucleotides, depending on the species. [score:1]
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25
[+] score: 5
They found that miR-320, miR-378, miR-211, miR-200a,b and miR-184 were significantly down-regulated during both stages of hibernation compared with non-hibernating animals, whereas miR-486, miR-451, miR-144 and miR-142 were significantly overexpressed in late torpor phase [22]. [score:5]
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26
[+] score: 4
miR-211 is a prosurvival microRNA that regulates chop expression in a PERK -dependent manner. [score:4]
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27
[+] score: 4
[5] miR-204 and miR-211 have been reported to act as vital negative regulators of Runx2 to promote adipogenesis and suppress osteogenesis in BMSCs. [score:4]
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28
[+] score: 4
Up-regulation of miR-33a [22, 23], miRNA-181b [24] and miR-211 [25] increased the sensitivity of PDAC cells to gemcitabine in vitro and in nude mice. [score:4]
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29
[+] score: 4
Other miRNAs from this paper: mmu-mir-30c-2, mmu-mir-455, mmu-mir-708
MiR-211, which is also induced after PERK activation, represses the CHOP transcription by targeting its 5′ untranslated region [6]. [score:4]
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30
[+] score: 3
Meanwhile miR-135b, miR-145b, miR-211, miR-3097, miR-3102 were significantly upregulated compared to that in wild type mouse lungs. [score:3]
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31
[+] score: 3
Intronic miR-211 assumes the tumor suppressive function of its host gene in melanoma. [score:3]
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32
[+] score: 3
The 10 most inhibited miRNAs are miR-1a, miR-133a/b, miR-196a, miR-206, miR-208b, miR-211, miR-592, miR-653, and miR-1963. [score:3]
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33
[+] score: 3
In the past few years, a number of studies of miRNAs in AD have emerged to support that deregulated miRNAs, such as miR-18b, miR-34c, miR-615, miR-211, miR-216 and miR-325, play important roles in the development and prognosis of AD [16]. [score:3]
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[+] score: 3
Furthermore, differential expression of miR-142-3p, miR-204, and miR-211 was also observed in urine samples between patient groups with chronic allograft dysfunction [47]. [score:3]
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35
[+] score: 3
Few inhibitory miRNAs were identified in melanoma, including miR-34a (uveal melanoma) [16], miR-193b [23], let-7a [24], and miR-211 [25], [26], while miR-182 [27] and miR-221/222 [28]were shown to stimulate metastatic potential of melanoma cells. [score:3]
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[+] score: 3
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-21, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-33a, hsa-mir-98, hsa-mir-29b-1, hsa-mir-29b-2, mmu-let-7g, mmu-let-7i, mmu-mir-27b, mmu-mir-29b-1, mmu-mir-30a, mmu-mir-30b, mmu-mir-126a, mmu-mir-133a-1, mmu-mir-135a-1, mmu-mir-141, mmu-mir-194-1, mmu-mir-200b, hsa-mir-30c-2, hsa-mir-30d, mmu-mir-30e, hsa-mir-203a, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-200b, mmu-mir-300, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-27b, hsa-mir-30b, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-135a-1, hsa-mir-135a-2, hsa-mir-141, hsa-mir-194-1, mmu-mir-30c-1, mmu-mir-30c-2, mmu-mir-30d, mmu-mir-200a, mmu-let-7a-1, mmu-let-7a-2, mmu-let-7b, mmu-let-7c-1, mmu-let-7c-2, mmu-let-7e, mmu-let-7f-1, mmu-let-7f-2, mmu-mir-21a, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-98, mmu-mir-326, rno-mir-326, rno-let-7d, rno-mir-343, rno-mir-135b, mmu-mir-135b, hsa-mir-200c, mmu-mir-200c, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-33, mmu-mir-29b-2, mmu-mir-135a-2, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-200a, hsa-mir-30e, hsa-mir-326, hsa-mir-135b, mmu-mir-133a-2, mmu-mir-133b, hsa-mir-133b, rno-let-7a-1, rno-let-7a-2, rno-let-7b, rno-let-7c-1, rno-let-7c-2, rno-let-7e, rno-let-7f-1, rno-let-7f-2, rno-let-7i, rno-mir-21, rno-mir-26b, rno-mir-27b, rno-mir-27a, rno-mir-29b-2, rno-mir-29a, rno-mir-29b-1, rno-mir-29c-1, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-33, rno-mir-98, rno-mir-126a, rno-mir-133a, rno-mir-135a, rno-mir-141, rno-mir-194-1, rno-mir-194-2, rno-mir-200c, rno-mir-200a, rno-mir-200b, rno-mir-203a, rno-mir-211, rno-mir-218a-2, rno-mir-218a-1, rno-mir-300, hsa-mir-429, mmu-mir-429, rno-mir-429, hsa-mir-485, hsa-mir-511, hsa-mir-532, mmu-mir-532, rno-mir-133b, mmu-mir-485, rno-mir-485, hsa-mir-33b, mmu-mir-702, mmu-mir-343, mmu-mir-466b-1, mmu-mir-466b-2, mmu-mir-466b-3, hsa-mir-300, mmu-mir-511, rno-mir-466b-1, rno-mir-466b-2, rno-mir-532, rno-mir-511, mmu-mir-466b-4, mmu-mir-466b-5, mmu-mir-466b-6, mmu-mir-466b-7, mmu-mir-466b-8, hsa-mir-3120, rno-mir-203b, rno-mir-3557, rno-mir-218b, rno-mir-3569, rno-mir-133c, rno-mir-702, rno-mir-3120, hsa-mir-203b, mmu-mir-344i, rno-mir-344i, rno-mir-6316, mmu-mir-133c, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-mir-30f, mmu-let-7k, mmu-mir-3569, rno-let-7g, rno-mir-29c-2, rno-mir-29b-3, rno-mir-466b-3, rno-mir-466b-4, mmu-mir-203b
miR-211 promotes cell growth by repressing lncRNA loc285194 expression. [score:3]
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[+] score: 2
miR-34b showed a similar pattern between the 4-cell and morula stages (Fig. 4e–f), and miR-140* and miR-211 showed similar patterns between the 8-cell and blastocyst stages of development (Fig. 4f–g and Table S7). [score:2]
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[+] score: 2
Other miRNAs from this paper: mmu-mir-873a, mmu-mir-873b
Only four microRNAs (microRNA-211, 290, 138-1 and 873) had the highest fold-change and the difference was statistically significant (P<0.05). [score:1]
Only microRNA-211 and micriRNA-873 (miR-873) satisfied these criteria. [score:1]
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39
[+] score: 1
Other miRNAs from this paper: mmu-mir-221
Additional experiments with a cardiac specific mutated c-Jun, would further provide additional evidence for our proposed role of Ang II in accentuating DCM via miR-211. [score:1]
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40
[+] score: 1
Indeed, it has been reported that multiple miRNAs participate in synaptic and cognitive impairment and AD-like neuropathology, including miR-9, miR-34, miR-132, miR-137, miR-188, miR-204, miR-211, and miR-212 [71– 77]. [score:1]
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41
[+] score: 1
We found that miR-211-3p, miR-494-3p, miR-669f-3p and miR–1907 may represent important miRNAs in GC–2 cells at a magnetic field intensity of 1 mT (Fig 5A). [score:1]
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[+] score: 1
Our previous work [8– 11] on rodent and primate mo dels demonstrated that MSC therapy enhanced the survival of cardiomyocytes, reduced myocardial fibrosis, and improved angiogenesis through paracrine effects, in which the factors secreted from MSCs, including leptin [12], miR-211 [8], and heparinase [9], played an important role in cardiac protection. [score:1]
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43
[+] score: 1
Other miRNAs from this paper: hsa-mir-211
2, 3, 4, 5 The micro deletion encompasses a region of ~1.5 MB from break-point (BP) 4 to BP5, with seven genes; MTMR10; FAN1; TRPM1; miR-211; KLF13; OTUD7A; and CHRNA7 (OMIM #612001). [score:1]
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44
[+] 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-26a-1, hsa-mir-26b, hsa-mir-27a, hsa-mir-29a, hsa-mir-32, hsa-mir-33a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, hsa-mir-107, mmu-let-7g, mmu-let-7i, mmu-mir-15b, mmu-mir-99a, mmu-mir-126a, mmu-mir-128-1, mmu-mir-130a, mmu-mir-140, mmu-mir-154, mmu-mir-204, mmu-mir-143, hsa-mir-204, hsa-mir-211, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-222, hsa-mir-223, mmu-mir-301a, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-128-1, hsa-mir-130a, hsa-mir-140, hsa-mir-143, hsa-mir-126, hsa-mir-129-2, hsa-mir-154, 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-26a-1, mmu-mir-26b, mmu-mir-29a, mmu-mir-29c, mmu-mir-27a, mmu-mir-129-2, mmu-mir-103-1, mmu-mir-103-2, mmu-mir-340, mmu-mir-107, mmu-mir-32, mmu-mir-218-1, mmu-mir-218-2, mmu-mir-223, mmu-mir-26a-2, mmu-mir-222, mmu-mir-128-2, hsa-mir-128-2, hsa-mir-29c, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-301a, hsa-mir-26a-2, hsa-mir-379, mmu-mir-379, hsa-mir-340, mmu-mir-409, hsa-mir-409, hsa-mir-499a, hsa-mir-455, hsa-mir-670, mmu-mir-1249, mmu-mir-670, mmu-mir-499, mmu-mir-455, bta-mir-26a-2, bta-mir-29a, bta-let-7f-2, bta-mir-101-2, bta-mir-103-1, bta-mir-16b, bta-mir-222, bta-mir-26b, bta-mir-27a, bta-mir-499, bta-mir-99a, bta-mir-126, bta-mir-128-1, bta-mir-34b, bta-mir-107, bta-mir-140, bta-mir-15b, bta-mir-218-2, bta-let-7d, bta-mir-29c, bta-mir-455, bta-let-7g, bta-let-7a-1, bta-let-7f-1, bta-let-7i, bta-mir-34c, bta-let-7a-2, bta-let-7a-3, bta-let-7b, bta-let-7c, bta-let-7e, bta-mir-103-2, bta-mir-204, hsa-mir-1249, hsa-mir-1306, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-128-2, bta-mir-129-2, bta-mir-130a, bta-mir-143, bta-mir-154a, bta-mir-211, bta-mir-218-1, bta-mir-223, bta-mir-26a-1, bta-mir-301a, bta-mir-32, bta-mir-33a, bta-mir-340, bta-mir-379, bta-mir-409a, bta-mir-670, mmu-mir-1306, bta-mir-1306, bta-mir-1249, bta-mir-2284i, bta-mir-2285a, bta-mir-2284s, bta-mir-2285d, bta-mir-2284l, bta-mir-2284j, bta-mir-2284t, bta-mir-2285b-1, bta-mir-2284d, bta-mir-2284n, bta-mir-2284g, bta-mir-2284p, bta-mir-2284u, bta-mir-2284f, bta-mir-2284a, bta-mir-2284k, bta-mir-2284c, bta-mir-2284v, bta-mir-2285c, bta-mir-2284q, bta-mir-2284m, bta-mir-2284b, bta-mir-2284r, bta-mir-2284h, bta-mir-2284o, bta-mir-2284e, hsa-mir-1260b, bta-mir-2284w, bta-mir-2284x, bta-mir-409b, hsa-mir-499b, bta-mir-1260b, bta-mir-2284y-1, bta-mir-2285e-1, bta-mir-2285e-2, bta-mir-2285f-1, bta-mir-2285f-2, bta-mir-2285g-1, bta-mir-2285h, bta-mir-2285i, bta-mir-2285j-1, bta-mir-2285j-2, bta-mir-2285k-1, bta-mir-2285l, bta-mir-6119, mmu-let-7j, bta-mir-2285o-1, bta-mir-2285o-2, bta-mir-2285n-1, bta-mir-2285n-2, bta-mir-2285p, bta-mir-2285m-1, bta-mir-2285m-2, bta-mir-2284y-2, bta-mir-2285n-3, bta-mir-2285n-4, bta-mir-2284y-3, bta-mir-154c, bta-mir-154b, bta-mir-2285o-3, bta-mir-2285o-4, bta-mir-2285m-3, bta-mir-2284y-4, bta-mir-2284y-5, bta-mir-2284y-6, bta-mir-2285m-4, bta-mir-2285o-5, bta-mir-2285m-5, bta-mir-2285n-5, bta-mir-2285n-6, bta-mir-2284y-7, bta-mir-2285n-7, bta-mir-2284z-1, bta-mir-2284aa-1, bta-mir-2285k-2, bta-mir-2284z-3, bta-mir-2284aa-2, bta-mir-2284aa-3, bta-mir-2285k-3, bta-mir-2285k-4, bta-mir-2284z-4, bta-mir-2285k-5, bta-mir-2284z-5, bta-mir-2284z-6, bta-mir-2284z-7, bta-mir-2284aa-4, bta-mir-2285q, bta-mir-2285r, bta-mir-2285s, bta-mir-2285t, bta-mir-2285b-2, bta-mir-2285v, bta-mir-2284z-2, mmu-let-7k, mmu-mir-126b, bta-mir-2285g-2, bta-mir-2285g-3, bta-mir-2285af-1, bta-mir-2285af-2, bta-mir-2285y, bta-mir-2285w, bta-mir-2285x, bta-mir-2285z, bta-mir-2285u, bta-mir-2285aa, bta-mir-2285ab, bta-mir-2284ab, bta-mir-2285ac, bta-mir-2285ad, bta-mir-2284ac, bta-mir-2285ae, chi-let-7a, chi-let-7b, chi-let-7c, chi-let-7d, chi-let-7e, chi-let-7f, chi-let-7g, chi-let-7i, chi-mir-103, chi-mir-107, chi-mir-1249, chi-mir-126, chi-mir-1306, chi-mir-130a, chi-mir-140, chi-mir-143, chi-mir-154a, chi-mir-154b, chi-mir-15b, chi-mir-16b, chi-mir-204, chi-mir-211, chi-mir-222, chi-mir-223, chi-mir-2284a, chi-mir-2284b, chi-mir-2284c, chi-mir-2284d, chi-mir-2284e, chi-mir-26a, chi-mir-26b, chi-mir-27a, chi-mir-29a, chi-mir-29c, chi-mir-301a, chi-mir-33a, chi-mir-340, chi-mir-34b, chi-mir-34c, chi-mir-379, chi-mir-409, chi-mir-455, chi-mir-499, chi-mir-99a, bta-mir-2285ag, bta-mir-2285ah, bta-mir-2285ai, bta-mir-2285aj, bta-mir-2285ak, bta-mir-2285al, bta-mir-2285am, bta-mir-2285ar, bta-mir-2285as-1, bta-mir-2285as-2, bta-mir-2285as-3, bta-mir-2285at-1, bta-mir-2285at-2, bta-mir-2285at-3, bta-mir-2285at-4, bta-mir-2285au, bta-mir-2285av, bta-mir-2285aw, bta-mir-2285ax-1, bta-mir-2285ax-2, bta-mir-2285ax-3, bta-mir-2285ay, bta-mir-2285az, bta-mir-2285an, bta-mir-2285ao-1, bta-mir-2285ao-2, bta-mir-2285ap, bta-mir-2285ao-3, bta-mir-2285aq-1, bta-mir-2285aq-2, bta-mir-2285ba-1, bta-mir-2285ba-2, bta-mir-2285bb, bta-mir-2285bc, bta-mir-2285bd, bta-mir-2285be, bta-mir-2285bf-1, bta-mir-2285bf-2, bta-mir-2285bf-3, bta-mir-2285bg, bta-mir-2285bh, bta-mir-2285bi-1, bta-mir-2285bi-2, bta-mir-2285bj-1, bta-mir-2285bj-2, bta-mir-2285bk, bta-mir-2285bl, bta-mir-2285bm, bta-mir-2285bn, bta-mir-2285bo, bta-mir-2285bp, bta-mir-2285bq, bta-mir-2285br, bta-mir-2285bs, bta-mir-2285bt, bta-mir-2285bu-1, bta-mir-2285bu-2, bta-mir-2285bv, bta-mir-2285bw, bta-mir-2285bx, bta-mir-2285by, bta-mir-2285bz, bta-mir-2285ca, bta-mir-2285cb, bta-mir-2285cc, bta-mir-2285cd, bta-mir-2285ce, bta-mir-2285cf, bta-mir-2285cg, bta-mir-2285ch, bta-mir-2285ci, bta-mir-2285cj, bta-mir-2285ck, bta-mir-2285cl, bta-mir-2285cm, bta-mir-2285cn, bta-mir-2285co, bta-mir-2285cp, bta-mir-2285cq, bta-mir-2285cr-1, bta-mir-2285cr-2, bta-mir-2285cs, bta-mir-2285ct, bta-mir-2285cu, bta-mir-2285cv-1, bta-mir-2285cv-2, bta-mir-2285cw-1, bta-mir-2285cw-2, bta-mir-2285cx, bta-mir-2285cy, bta-mir-2285cz, bta-mir-2285da, bta-mir-2285db, bta-mir-2285dc, bta-mir-2285dd, bta-mir-2285de, bta-mir-2285df, bta-mir-2285dg, bta-mir-2285dh, bta-mir-2285di, bta-mir-2285dj, bta-mir-2285dk, bta-mir-2285dl-1, bta-mir-2285dl-2, bta-mir-2285dm
Among these, 16 precursors were found amongst the 43 conserved between human, mouse, cow and goat in our analysis (let-7 g, mir-101-2, mir-103, mir-107, mir-128-1, mir-1306, mir-140, mir-15b, mir-16b, mir-211, mir-218-1, mir-26a-1, mir-32, mir-33a, mir-455, let-7-2), so the location of these precursors appears to be highly conserved in all vertebrates. [score:1]
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