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80 publications mentioning hsa-mir-376c

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-376c. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

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[+] score: 293
MiR-376c target identification by proteomic analysisWe performed a proteomic analysis to identify proteins whose expression was altered in miR-376c -overexpressing HuCCT1 cells, some of which may be targets of miR-376c. [score:9]
Downregulation of miR-376c expression levels in bile duct carcinoma cell lines, and proteomic analysis of miR-376c -overexpressing HuCCT1. [score:8]
Saito et al. reported the miRNA expression profile of T24 bladder cancer cells treated with 5-AZA-dCR and the HDAC inhibitor 4-phenylbutyric acid, and showed that miR-376c was one of the miRNAs upregulated after treatment [35]. [score:8]
Our results demonstrated that GRB2, an in silico miR-376c target candidate, was significantly downregulated in miR-376c -overexpressing HuCCT1 cells. [score:8]
After 3 days, the histone deacetylase (HDAC) inhibitor trichostatin A (TSA, Sigma-Aldrich; 0.1, 0.5, or 1.0 µM) was added and cells were cultured for a further 24 h. MiR-376c is downregulated in CC cell lines including HuCCT1We previously performed small RNA sequencing using HuCCT1 and HIBEpiC to reveal differential miRNA expression [18]. [score:8]
Enforced expression of miR-376c significantly impaired migration of HuCCT1 cells by reducing levels of the targeted mRNA, indicating that downregulation of miR-376c is critical for this response. [score:8]
0069496.g001 Figure 1Downregulation of miR-376c expression levels in bile duct carcinoma cell lines, and proteomic analysis of miR-376c -overexpressing HuCCT1. [score:8]
We found 41 protein spots with significant differences in intensity between controls and Pre-miR-376c -transfected HuCCT1 cells (upregulation or downregulation by more than 1.2-fold, P≤0.011). [score:7]
Numbers below the upregulation (red) and downregulation (green) symbols represent the fold changes by Pre-miR-376c treatment; numbers in parentheses represent the fold changes by siGRB2-2 treatment. [score:7]
MiR-376c expression is regulated by epigenetic control in HuCCT1To determine whether miR-376c expression was dysregulated by epigenetic alterations in HuCCT1 cells, we first assessed the methylation status of the 6 CpG sites (sites I–VI) located 85 to 202 bp upstream of miR-376c; i. e., in the putative promoter region, in HIBEpiC and HuCCT1 cells by bisulfite genome sequencing (Figure 5A). [score:7]
To elucidate key molecules in EGF -dependent HuCCT1 migration, in which GRB2 upregulation is caused by abnormal suppression of miR-376c, we compared expression profiles of mRNAs affected by Pre-miR-376c and siGRB2 (siGRB2-2) in EGF -treated HuCCT1 cells. [score:7]
We focused on the downregulated proteins as potential direct targets of miR-376c (Table 1). [score:7]
We performed a proteomic analysis to identify proteins whose expression was altered in miR-376c -overexpressing HuCCT1 cells, some of which may be targets of miR-376c. [score:7]
analysis revealed that miR-376c, which was highly expressed in HIBEpiC, was significantly downregulated in all CC cell lines examined in this study (Figure 1A). [score:6]
Proteins downregulated by miR-376c overexpression in HuCCT1 cells in proteomic analysis. [score:6]
The target site corresponding to the seed sequence of miR-376c was converted via mutation; the mutation introduced into the miR-376c recognition site of GRB2 3'-UTR in the reporter plasmid is also shown. [score:5]
The GRB2 protein predicted by TargetScan as a target of miR-376c is shown in bold. [score:5]
We reported previously that miR-376c (formerly designated as miR-368 in miRBase Release 12; currently designated as miR-376c-3p in miRBase Release 19) was expressed in a normal intrahepatic biliary epithelial cell line (HIBEpiC), but was significantly suppressed in an ICC cell line (HuCCT1) [18]. [score:5]
To test this hypothesis, we sought the targets of this miRNA, and characterized the effect of miR-376c down-regulation in HuCCT1 cells. [score:4]
Conversely, in normal intrahepatic biliary epithelial cells, the expression of miR-376c might regulate the amount of GRB2 protein and cell migration. [score:4]
Two reports of miR-376c upregulation in a subset of acute myeloid leukemia samples have been published [38], [39]. [score:4]
However, the biological significance of the downregulation of miR-376c in HuCCT1 cells was unknown. [score:4]
A spot downregulated by treatment with Pre-miR-376c is indicated by the arrow, which was later shown by mass spectrometry to be GRB2. [score:4]
Table S2 Genes upregulated by Pre-miR-376c and siGRB2-2. (XLS) Click here for additional data file. [score:4]
In migration experiments using Pre-miR-376c and siGRB2s, downregulation of GRB2 protein was shown to reduce EGF -dependent migration of HuCCT1 cells. [score:4]
It is likely that miR-376c is downregulated specifically in bile duct carcinoma cell lines. [score:4]
Down-regulation of miR-376c allowed an increase in the amount of GRB2 protein, resulting in acceleration of HuCCT1 migration. [score:4]
Combination treatment with 5-AZA-dCR and TSA showed that miR-376c was significantly upregulated (Figure 5C, number 7 and 8). [score:4]
Here, we focused on functional studies of miR-376c, which is significantly downregulated in CC cell lines. [score:4]
Table S1 Genes downregulated by Pre-miR-376c and siGRB2-2. (XLS) Click here for additional data file. [score:4]
From the viewpoint of the cellular function of miR-376c, two down-regulated genes; i. e., interleukin-1 beta (IL1B) and matrix metallopeptidase 9 (MMP9), were associated primarily with several cellular-movement networks in the Ingenuity Knowledge Base (Table S3). [score:4]
These results indicate that the synergistic effects of DNA demethylation and histone acetylation are responsible for regulation of miR-376c expression. [score:4]
To determine whether miR-376c expression was dysregulated by epigenetic alterations in HuCCT1 cells, we first assessed the methylation status of the 6 CpG sites (sites I–VI) located 85 to 202 bp upstream of miR-376c; i. e., in the putative promoter region, in HIBEpiC and HuCCT1 cells by bisulfite genome sequencing (Figure 5A). [score:4]
These results suggest that miR-376c regulates EGF -dependent cell migration through repression of GRB2 translation. [score:4]
Furthermore, in this study, we demonstrated that IL1B and MMP9 were significantly downregulated in HuCCT1 cells treated with Pre-miR-376c or siGRB2. [score:4]
We identified a direct target mRNA of miR-376c by proteomic analysis. [score:4]
Moreover, a confirmed that miR-376c repressed the translation of GRB2 in a seed-sequence -dependent manner in HuCCT1 cells (Figure 2). [score:3]
MiR-376c expression is regulated by epigenetic control in HuCCT1. [score:3]
Expression profiles of mRNAs affected by Pre-miR-376c and siGRB2-2 in EGF -treated HuCCT1 cells were conducted by microarray analysis. [score:3]
0069496.g002 Figure 2 Validation of GRB2 as a miR-376c Target. [score:3]
Mechanisms controlling miR-376c gene expression have not been reported. [score:3]
In the present study, we revealed that epigenetic repression of miR-376c accelerated EGF -dependent cell migration by targeting GRB2 in HuCCT1 cells. [score:3]
Furthermore, as shown in Figure 2B, the GRB2 mRNA level was also significantly decreased by Pre-miR-376c overexpression. [score:3]
In this study, combination treatment with 5-AZA-dCR and TSA significantly induced the expression of miR-376c in HuCCT1 cells (Figure 5C), suggesting epigenetic, including histone, modification. [score:3]
We hypothesized that miR-376c could function as a tumor suppressor in these cells. [score:3]
Next, to determine whether the 3′-UTR of GRB2 is a direct target of miR-376c, we performed a luciferase reporter assay. [score:3]
Validation of GRB2 as a miR-376c Target. [score:3]
Taken together, these results suggest that GRB2 is a target of miR-376c in HuCCT1 cells. [score:3]
In summary, we have shown that GRB2 -targeted miR-376c is epigenetically repressed in HuCCT1 cells, resulting in acceleration of cell migration by EGF signaling enhancement via GRB2. [score:3]
HuCCT1 cells were transfected with the pMIR-GRB2, pMIR-GRB2mt, or the control vector pRL-TK (Renilla luciferase expression plasmid), together with Pre-miR-376c or the Pre-miR -negative control at 10 nM, using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA) in 24-well plates. [score:3]
Our data suggest that DNA methylation and HDAC modification suppress the transcription of miR-376c in these cells. [score:3]
0069496.g004 Figure 4. (A) Venn diagrams showing the significantly different mRNA expression levels of Pre-miR-376c and siGRB2-2 transfectants of HuCCT1 relative to appropriate controls. [score:3]
However, the target genes and functions of miR-376c in biliary epithelial cells have been not reported. [score:3]
Validation of GRB2 as a miR-376c TargetTo confirm the 2D-DIGE results, we performed analysis of HuCCT1 transfected with Pre-miR-376c. [score:3]
Although the expression and function of RhoU in bile duct cells are unknown, miR-376c may modulate EGF -mediated signaling through physical interaction between RhoU and GRB2. [score:3]
Microarray analysis showed that changes in expression of 1148 and 2733 genes were induced by Pre-miR-376c and siGRB2-2, respectively. [score:3]
MiR-376c regulates epidermal growth factor (EGF) -dependent migration of HuCCT1 via GRB2GRB2 is known to be a key molecule in intracellular signal transduction through the EGF receptor (EGFR), and can be overexpressed in tumors of breast and bladder cancers [24]– [26]. [score:3]
MiR-376c is downregulated in CC cell lines including HuCCT1. [score:3]
MiR-376c expression was increased slightly by 5-AZA-dCR or TSA treatment alone (Figure 5C, number 4 and 5). [score:2]
MiR-376c target identification by proteomic analysis. [score:2]
As shown in Figure 2D, Pre-miR-376c overexpression decreased significantly the luciferase activity in HuCCT1 cells cotransfected with pMIR-GRB2 (by ∼30% compared to the negative control), but not significantly in cells cotransfected with pMIR-GRB2mt, a reporter plasmid mutated in the putative miR-376c recognition site of the GRB2 3′-UTR (Figure 2C). [score:2]
Thus, we evaluated the gene suppression of IL1B and MMP9 in HuCCT1 cells treated with Pre-miR-376c and siGRB2-2. Pre-miR-376c significantly decreased (to 66%) expression of IL1B (Figure 4C) and MMP9 (to 52%, Figure 4D), compared to Pre-miR -negative controls. [score:2]
The numbers of genes regulated by Pre-miR-376c and siGRB2-2 are indicated. [score:2]
Methylation of miR-376c. [score:1]
In addition, we assessed the effect of Pre-miR-376c and siGRB2 transfection on cell growth (Figure S1). [score:1]
Figure S1 The effects of Pre-miR-376c and siGRB2s transfection on cell growth. [score:1]
Reporter vector (pMIR-GRB2 [GRB2] or pMIR-GRB2mt [GRB2mt]) and Pre-miR molecule (Pre-miR-376c [376c] or Pre-miR negative control [NC]) were co -transfected into HuCCT1 cells. [score:1]
To construct a reporter plasmid with a mutated miR-376c recognition site of GRB2 3′-UTR, an inverse PCR method was used. [score:1]
For further characterization of miR-376c expression in CC cell lines, the ICC cell lines TKKK, Huh28, and IHGGK, and the extrahepatic CC cell line TFK-1 were examined. [score:1]
Small RNA sequencing showed that miR-376c was found exclusively in HIBEpiC and not in HuCCT1 (i. e., cloning frequency >0.1% in HIBEpiC and 0.0% in HuCCT1) [18]. [score:1]
MiR-376c regulates epidermal growth factor (EGF) -dependent migration of HuCCT1 via GRB2. [score:1]
Kawahara et al. showed that miR-376 transcripts were subject to RNA editing, converting adenosine to inosine in a tissue -dependent manner, leading to a change in the silenced gene set [36]. [score:1]
To confirm the 2D-DIGE results, we performed analysis of HuCCT1 transfected with Pre-miR-376c. [score:1]
MiR-376c belongs to the miR-376 cluster gene family, containing miR-376a, miR-376a*, and miR-376b. [score:1]
We did not, however, observe an effect of miR-376c on cell growth in this cancer cell type (Figure S1). [score:1]
HuCCT1 cells grown to semi-confluence were transfected with Pre-miR-376c (mature miR-376c-3p mimic) or Pre-miR negative control #1 (Applied Biosystems, Foster City, CA, USA) at a final concentration of 30 nM using Lipofectamine 2000 (Invitrogen, Carlsbad, CA, USA), according to the manufacturer's protocol. [score:1]
Cells were harvested 72 h after the initiation of transfection of Pre-miR-376c or the Pre-miR -negative control, and subjected to proteomic analysis. [score:1]
Although our experiments were conducted with an ICC cell line mo del in vitro, our findings on miR-376c function provide a new insight into pathophysiology of ICC. [score:1]
Treatment with Pre-miR-376c significantly decreased EGF -induced migration (to 57% of the control value, Figure 3A). [score:1]
Data are presented as the ratio of the number of migrating Pre-miR-376c (376c) -transfected cells to that of cells transfected with the Pre-miR -negative control (NC), in the presence or absence of EGF. [score:1]
0069496.g005 Figure 5Methylation of miR-376c. [score:1]
We also found that CpG sites upstream of the miR-376c gene were highly methylated in HuCCT1 cells. [score:1]
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[+] score: 118
Introduction of the IGF1R-3'UTR-luciferase vector into mir-376a -transfected or mir-376c -transfected cells led to a significant ~83% and ~65% decrease in the level of luciferase expression relative to the same cells following introduction with a control luciferase vector, respectively, indicating that the stable expression of both miRNAs leads to further significant down-regulation on the 3'UTR of IGF1R (Figure  4D), thus establishing IGF1R as a target of both mir-376a and mir-376c. [score:10]
To assess whether the down-regulation of IGF1R by mir-376a and mir-376c could account for the observed biological phenotype in these cells, IGF1R was pharmacologically inhibited using the commercially-available IGF1R inhibitor AG-1024 [26]. [score:8]
We therefore decided to focus on other miRNAs whose expression was shown to be down-regulated but not entirely absent in melanoma and as a first step generated melanoma cell lines that ectopically express either mir-376a or mir-376c (Figure  3A). [score:8]
Our results suggest that down-regulation of mir-376a and mir-376c may contribute to IGF1R over -expression and to aberrant negative regulation of this signaling pathway in melanoma, thus promoting tumorigenesis and metastasis. [score:7]
In our experimental system, IGF1R levels were higher in melanoma cell lines than in normal melanocytes, and the ectopic expression of mir-376a and mir-376c led to down-regulation of the receptor. [score:6]
The work presented here demonstrates that mir-376a and mir-376c negatively regulate IGF1R, and suggests that aberrations in this regulatory mechanism, in the form of down-regulation of mir-376a/c, take part in melanoma progression and metastasis. [score:6]
Moreover, Philippidou et al. also observed that both mir-127-3p and mir-376c are down-regulated in a metastatic cell line relative to their expression in the primary tumor from the same patient [5], again in agreement with our current observations. [score:6]
Stable over -expression of mir-376a and mir-376c, two miRNAs from this cluster that could be re-expressed following epigenetic manipulation, led to modest growth retardation and to a significant decrease in migration in-vitro. [score:5]
IGF1R inhibition by AG-1024 pheno-copied the decrease in migration seen following over -expression of either mir-376a or mir-376c using the same experimental system, in a dose -dependent manner (Figure  4E). [score:5]
Pharmacological inhibition of IGF1R pheno-copied the decrease in migration seen following mir-376a and mir-376c over -expression, suggesting that down-modulation of the IGF1R signaling pathway may be responsible for the observed anti-migratory effect of these miRNAs in melanoma cell lines. [score:5]
Four of these five miRNAs (mir-127-3p, mir-136, mir-376a and mir-376c) were found to be down-regulated but not entirely silenced in nevi and melanoma (Additional file 2). [score:4]
Four of these miRNAs (namely mir-127-3p, mir-136, mir-376a and mir-376c) were shown to be down-regulated but not completely silenced in nevi and melanomas. [score:4]
Indeed, stable expression of mir-376a and mir-376c in melanoma cells led to a decrease in IGF1R and protein, and a luciferase reporter assay indicated that the 3'UTR of IGF1R is a target of both mir-376a and mir-376c. [score:4]
Luciferase reporter assays indicate that, as bioinformatically predicted, mir-376a and mir-376c directly target IGF1R. [score:3]
Figure 3 The effect of stable expression of mir-376a and mir-376c on the proliferation and migration of melanoma cells. [score:3]
The administration of AG-1024 to melanoma cells over -expressing either mir-376a or mir-376c did not lead to a further decrease in their migration (results not shown), suggesting that the IGF1R axis could not be further modulated to decrease migration. [score:3]
Cells over -expressing either mir-376a or mir-376c exhibited attenuated growth relative to pTER -transfected control cells (Figure  3B). [score:3]
AG-1024 did not lead to decreased cellular proliferation in either the control cells or the cells over -expressing mir-376a or mir-376c, suggesting that the modest effect of these miRNAs on cellular growth is mediated through different mechanisms. [score:3]
Stable expression of mir-376a or mir-376c led to a decrease in IGF1R levels both at the and at the protein levels (Figure  4C). [score:3]
We provide data showing that re -expression of mir-376a and mir-376c, two miRNAs from this cluster, lead to attenuation of melanoma proliferation and migration. [score:3]
The sequence conservation from human to lizard in the vicinity of mir-376c and 376a seed sequences and the putative interaction of the miRNAs and the are shown (taken from TargetScan at http://www. [score:3]
Ectopic expression of mir-376a and mir-376c had a modest yet significant effect on cell growth, but a profound effect on cellular migration in-vitro. [score:3]
Nonetheless, the inhibition of IGF1R by mir-376a and mir-376 has not been described before. [score:3]
This vector was then introduced into melanoma cells over -expressing mir-376a, mir-376c or a control vector (designated pTER). [score:3]
obtained with the more sensitive method of qRT-PCR verified that mir-376a, mir-376c and mir-136 can be significantly induced following treatment with epigenetic modifiers in most of the melanoma cell lines (Figure  2E and results not shown). [score:1]
The putative binding site of mir-376c is classified as ‘7mer-8mer binding’, and that of mir-376a is classified as ‘8mer binding’. [score:1]
Bioinformatic analysis using several web -based tools showed that miRNA-376a and miRNA-376c have putative binding sites at the 3'UTR of IGF1R (Figure  4A), a tyrosine kinase receptor long known to be implicated in melanoma tumorigenesis and progression [23]. [score:1]
Whereas pTER -transfected control melanoma cells exhibited a time -dependent migration through the membrane, the mir-376a and mir-376c transfected cells showed almost no migration through the membrane within a 24 h period (Figure  3E). [score:1]
Mir-376a and mir-376c transfected cells showed significantly attenuated migration through a transwell membrane 24 hours after seeding relative to pTER -transfected control cells (Figure  3D). [score:1]
Both mir-376a and mir-376c pre-miRNAs were cloned into the pTER plasmid [47, 48]. [score:1]
Interestingly, out of all 65 chromosome-14-miRNAs assessed in four melanoma cell lines, only five miRNAs were shown to be induced in any of the cell lines: mir-127-3p, mir-137, mir-376a (also designated mir-376a-3p), mir-376c and mir-485-3p. [score:1]
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[+] score: 100
More importantly, xenograft experiment indicated that gastric tumor growth was inhibited when the tumors were overexpressed in gastric cancer cells, suggesting that hsa-miR-376c-3p may serve as a tumor suppressor gene in gastric cancer. [score:7]
Overexpression of hsa-miR-376c-3p Inhibited the Gastric Tumor Growth In Vivo. [score:5]
Inhibitor negative control and hsa-miR-376c-3p inhibitor miRNA were purchased from ABM (Canada). [score:5]
This process was correlated with the increasing expression of BAD and decreasing expression of BCL-2. This suggested that hsa-miR-376c-3p induced apoptosis was mediated by BCL-2/BAD death pathway. [score:5]
Besides, the western blotting data showed that overexpression of hsa-miR-376c-3p increased the expression of BAD and smad4 and decreased the antiapoptotic gene BCL-2 (Figure 4(b)). [score:5]
In this study, we used hsa-miR-376c-3p inhibitor and overexpression construct to elucidate the role of hsa-miR-376c-3p in the gastric cancer cell apoptosis. [score:5]
Constructs of hsa-miR-376c-3p Inhibitor and Overexpression Plasmid. [score:5]
Besides, immunostaining result further confirmed expression alteration in smad4, BAD, and BCL-2 when hsa-miR-376c-3p was overexpressed (Figure 5). [score:5]
Overexpression of hsa-miR-376c-3p Inhibited the Gastric Tumor Growth In Vivo Next, we detected the effect of hsa-miR-376c-3p on gastric tumor growth in vivo. [score:5]
BAD/BCL-2 signaling was involved in hsa-miR-376c-3p -mediated apoptosis Furthermore, we found the regulation of hsa-miR-376c-3p could alter the expression level of some cancer-related genes. [score:4]
Collectively, these results indicated that hsa-miR-376c-3p expression regulated the gastric tumor cell growth in vitro through BAD/BCL-2 pathway. [score:4]
BAD/BCL-2 signaling was involved in hsa-miR-376c-3p -mediated apoptosisFurthermore, we found the regulation of hsa-miR-376c-3p could alter the expression level of some cancer-related genes. [score:4]
In the future, the development of hsa-miR-376c-3p as a novel therapeutic target for the treatment of gastric cancer may be applicable. [score:4]
Since hsa-miR-376c-3p was expressed in the gastric adenocarcinoma cell line SGC-7901, we determined whether the regulation of hsa-miR-376c-3p affected the cell viability. [score:4]
Furthermore, our in vitro data showed that hsa-miR-376c-3p overexpression could lead to the promotion of apoptosis and G1 arrest in gastric cancer cells. [score:3]
Expression of hsa-miR-376c-3p in Tumor Samples from Gastric Cancer Patients. [score:3]
Furthermore, we also indicated that overexpression of hsa-miR-376c-3p had an antigastric tumor effect in vivo. [score:3]
The quantitative reverse transcription PCR result indicated that both hsa-miR-376c-3p and smad4 were expressed in the gastric cancer cell line (Figure 1(a)). [score:3]
To elucidate the role of hsa-miR-376c-3p in gastric tumor growth, we firstly determined the expression level of hsa-miR-376c-3p and smad4 in four cell lines. [score:3]
This raised the possibility that hsa-miR-376c-3p was a new target and provided a new strategy to treat malignant tumors, including gastric cancer. [score:3]
From this study, a previously unidentified miRNA hsa-miR-376c-3p was shown to be closely correlated with gastric cancer development and progression. [score:2]
The real time PCR results indicated that the expression level of hsa-miR-376c-3p was significantly lower in tumor tissues compared to the tissues adjacent to tumors (Figure 6(a)). [score:2]
Xenograft of SGC-7901 cells transfected with empty vector did not change the tumor size, while the overexpression of hsa-miR-376c-3p negatively affected the in vivo tumor growth compared to the controls (Figure 4(a)). [score:2]
The hsa-miR-376c-3p overexpression group exhibited the enhanced cell apoptosis (Figure 1(b)) and increases the cell ratio at G1 phase (Figure 2(a)) compared to the nontransfected group (Figures 1(c) and 2(b)) and empty vector group (Figures 1(d) and 2(c)); however, there is no significant difference. [score:2]
3.1. hsa-miR-376c-3p Regulated SGC-7901 Cell Apoptosis. [score:2]
We found that regulation of hsa-miR-376c-3p played role in the tumor cell growth both in vitro and in vivo. [score:2]
Sequence of hsa-miR-376c-3p was cloned into PCI vector. [score:1]
Further study will be focused on clarifying more specific mechanisms underlying the roles of hsa-miR-376c-3p in the progression and invasion of gastric cancer as well as to assess its function in clinical context. [score:1]
Next, we detected the effect of hsa-miR-376c-3p on gastric tumor growth in vivo. [score:1]
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[+] score: 70
Coincidently, our target gene analysis showed that all the 4 up-regulated miRNAs (miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p) target TP53, cyclin -dependent kinase inhibitor 1A (CDKN1A) and cyclin -dependent kinase inhibitor 2A (CDKN2A). [score:12]
The up-regulated and down-regulated miRNAs (miR-20b, miR-92a-3p, miR-92b, miR-376c-3p, miR-150, miR-342-3p, and miR-663) may be involved in the regulation of transcription, DNA -dependent positive regulation of transcription from RNA polymerase II promoter, protein amino acid phosphorylation, and negative regulation of transcription from RNA polymerase II promoter. [score:10]
Moreover, the up-regulated miRNAs (miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p) target BH3-interacting domain (BID), TP53 and PTEN. [score:6]
d Main pathways influenced by genes targeted by two or more miRNAs from miR-19b, miR-101, and miR-199a-5p Pathway analysis showed that the predicted target genes related to miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p were involved in regulation of actin cytoskeleton, focal adhesion, MAPK signaling pathway, calcium signaling pathway, and axon guidance (Fig.   5c). [score:6]
showed that the most significant biological processes targeted by at least two of various miRNAs (miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p) were regulation of transcription, DNA -dependent positive regulation of transcription from RNA polymerase II promoter, protein amino acid phosphorylation, negative regulation of transcription from RNA polymerase II promoter, and G1/S transition of mitotic cell cycle (Fig.   5a). [score:6]
d Main pathways influenced by genes targeted by two or more miRNAs from miR-19b, miR-101, and miR-199a-5p Pathway analysis showed that the predicted target genes related to miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p were involved in regulation of actin cytoskeleton, focal adhesion, MAPK signaling pathway, calcium signaling pathway, and axon guidance (Fig.   5c). [score:6]
Our data indicates that the unique 7 miRNAs (miR-150, miR-342-3p, miR-663, miR-20b, miR-92a-3p, miR-376c-3p and miR-92b) expression signature could be involved in the development of HBV- related HCC, suggesting interesting potential novel therapeutic options. [score:4]
By miRNA expression profile, we found that miR-150, miR-342-3p, miR-663, miR-20b, miR-92a-3p, miR-376c-3p, and miR-92b are specifically altered in HBV-related HCC. [score:3]
a Relationship among target genes predicted by miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p. [score:3]
c Main pathways influenced by genes targeted by two or more miRNAs from miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p. [score:3]
a Main biological processes influenced by genes targeted by two or more miRNAs from miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p. [score:3]
IPA-obtained network showing the relationships among 6 co-regulated miRNAs (miR-150, miR-342-3p, miR-92a-3p, miR-92b, and miR-376c-3p) To evaluate the effect of HBV infection on the change in expression of miRNAs, 12 pairs of samples from HCC and non-tumor tissues (including 6 HBV -positive HCC and 6 HBV -negative HCC and their non-tumor tissues) were collected. [score:2]
IPA-obtained network showing the relationships among 6 co-regulated miRNAs (miR-150, miR-342-3p, miR-92a-3p, miR-92b, and miR-376c-3p) HBV infection is a major health problem that leads to a significant rise in mortality and is reported to be closely related to HCC [20]. [score:2]
Ultimately, miR-20b, miR-92a-3p, miR-92b, miR-376c-3p, miR-150, miR-342-3p, and miR-663 were selected. [score:1]
Eight miRNAs (miR-223, miR-98, miR-15b, miR-199a-5p, miR-19b, miR-22, miR-451, and miR-101) were involved in HBV-unrelated HCC, 5 miRNAs (miR-98, miR-375, miR-335, miR-199a-5p, and miR-22) were involved in HBV infection, and 7 miRNAs (miR-150, miR-342-3p, miR-663, miR-20b, miR-92a-3p, miR-376c-3p and miR-92b) were specifically altered in HBV-related HCC. [score:1]
In our IPA results, the 6 selected miRNAs (miR-150, miR-342-3p, miR-20b, miR-92a-3p, miR-92b, and miR-376c-3p) are shown to comprise a network which linked themselves among AGO2, DICER1, BCL2L11, CCND1, CCND2, CCNE1, CDK7, E2F1, E2F3, TP53, and four other genes (Fig.   6). [score:1]
The identity of the 12 miRNAs is as follows: miR-21, miR-20b, miR-92a-3p, miR-92b, miR-376c-3p, miR-150, miR-451, miR-101, miR-424, miR-342-3p, miR-122a, and miR-663. [score:1]
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5
[+] score: 65
While NFAT5 mRNA levels were not significantly affected by overexpression of hsa-miR-516b, overexpression of hsa-miR-376c or has-miR-486-5p did result in down-regulation of NFAT5, with has-miR-486-5p having the most significant effect (P = 0.0411). [score:8]
In LTBI individuals hsa-miR-516b was up-regulated, while hsa-miR-376c was down-regulated. [score:7]
In addition, hsa-miR-196b and hsa-miR-376c shared the same eight target mRNAs, while hsa-miR-376c, hsa-miR-516b and hsa-miR-486-5p all targeted NFAT5 whose gene and protein expression are known to be strongly induced by M. tuberculosis [16]. [score:7]
from Solexa sequencing suggested that hsa-miR-516b, hsa-miR-196b and hsa-miR-376c are significantly up-regulated in patients with active TB, while hsa-miR-486-5p is significantly down-regulated. [score:7]
Results from Solexa sequencing suggested that hsa-miR-516b, hsa-miR-196b and hsa-miR-376c are significantly up-regulated in patients with active TB, while hsa-miR-486-5p is significantly down-regulated. [score:7]
For example, both hsa-miR-376c and hsa-miR-516b had 11 targets in common, while hsa-miR-376c and hsa-miR-486-5p had 12 targets in common. [score:5]
Although results for hsa-miR-486-5p and hsa-miR-516b were not consistent with those from RNA-Seq (Figure 4 ), hsa-miR-196b was consistently significantly up-regulated in serum from patients with active TB compared with the other three groups using both techniques, and expression of hsa-miR-376c was significantly higher in serum from TB patients than in serum from individuals with LTBI and un-inoculated healthy individuals, suggesting that these two microRNAs have potential as diagnostic markers. [score:5]
We overexpressed three miRNAs predicted to target NFAT5 (hsa-miR-376c, hsa-miR-516b and hsa-miR-486-5p) in HEK293 cells and analysed their transcript levels. [score:5]
These results suggest that hsa-miR-376c and has-miR-486-5p may be involved in regulating the NFAT5 pathway, possibly leading to the higher levels of NFAT5 expression observed in patients with active TB [16]. [score:4]
Hsa-miR-196b and hsa-miR-376c were up-regulated in TB patients in comparison with each of the other three groups. [score:4]
Hsa-miR-516b, hsa-miR-486-5p and hsa-miR-376c all target NFAT5 (nuclear factor of activated T-cells 5) (http://ferrolab. [score:3]
Figure 2 shows the microRNA-Gene-Network for miRNAshsa-miR-516b,hsa-miR-196b, hsa-miR-376c and hsa-miR-486-5p. [score:1]
microRNA-gene network for hsa-miR-196b, hsa-miR-516b, hsa-miR-376c and hsa-miR-486-5p. [score:1]
Hsa-miR-376c, first reported by Sylvius et al [36] is associated with muscular dystrophy [33]. [score:1]
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6
[+] score: 34
The most highly up-regulated miRNAs were miR-23b (+6.8) and miR-376c (+7.0), while miR-494 (–9.8) and miR-487b (–11.6) were the most down-regulated miRNAs (Table 1). [score:7]
Thus miR-98, miR-323-3p, miR-330-3p, miR-376a, miR-494, miR-598 were down-regulated by UVA and UVB, while miR-191, miR-376c and miR-501-5p were up-regulated by both. [score:7]
Of the 3 up-regulated miRNAs after UVA- and UVB-irradiation (miR-191, mir-376c, miR-501) miR-191 and miR-376c shared the same regulatory element GLYCA-nTRE (gcaggtgaggacttca), which belongs to thyroid regulatory elements (TREs ), whereas miR-376c and miR-501-5p shared GATA-1-undefined-site-13 (cccacccac). [score:6]
As input the up-regulated miRNA-set consists of miR-191, miR-376c and miR-501-5p. [score:4]
The highest up-regulated miRNAs are miR-376c (+7.0, UVA; +2.3, UVB) and miR- 501-5p (+2.1, UVA; +6.8, UVB). [score:4]
In detail we confirmed the up-regulation of miR-23b (UVA), miR-361-5p (UVB), miR-191 (UVA and UVB) and miR-376c (UVA and UVB). [score:4]
Thyroid hormone receptor T3R is the only identified regulatory factor for GLYCA-nTRE (gcaggtgaggacttca) (shared by miR-191 and miR-376c, see above) [35]. [score:2]
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7
[+] score: 31
About 14% (8/56) of the miR-374a validated target mRNAs also encoded aging -associated proteins, as well as ~8% (1/12) of the miR-376c targets, ~7% (3/41) of the miR-211 targets, and ~7% (10/146) of the miR-340 targets. [score:9]
miR-374 was also downregulated in older participants in an earlier study [18], but in contrast with our study, miR-376 was upregulated in older participants in another report [20]. [score:7]
miR-374a-5p, miR-340-3p, and miR-376c-3p all had negative correlations and were similarly downregulated in the longer-lived subgroup but upregulated in the shorter lived subgroup. [score:7]
Additionally, both IGF1R mRNA (a miR-376c target) and IGF2R mRNA (a miR-211 target) encode receptors of the insulin signaling pathway (IGF1R and IGF2R, respectively), which has been tightly linked to variation in human longevity[35, 36]. [score:5]
Interestingly, none of the six miRNAs has previously been shown to play a mechanistic role in aging, and none has been implicated in heart disease, but many have been shown to function and/or act as biomarkers in different cancers (miR-211: melanoma cell invasive-ness; head, neck, renal cell carcinomas; pancreatic cancer; miR-374: small cell lung cancer; miR-340: osteosarcoma, colorectal cancer, breast cancer, gastric cancer; miR-376: glioblastoma, hepato-cellular carcino-ma) [24]. [score:3]
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8
[+] score: 29
Upregulation of TGFA expression in osteosarcoma tissues and cells and its correlation with MIR376A and MALAT1 TGFA is a direct target of MIR376C, one of the MIR376 family members that regulate OS cell growth [18]. [score:10]
Inverse correlation of MIR376A and MALAT1 expression in osteosarcoma tissues and direct interaction between MIR376A and the 3′UTR of MALAT1 in vitroAccording to previous studies, MIR376 family members play a suppressive role in OS [18, 19]. [score:6]
TGFA is a direct target of MIR376C, one of the MIR376 family members that regulate OS cell growth [18]. [score:5]
It has been reported that TGFA regulates OS cell growth as a direct target of MIR376C, one of the MIR376 family members [18]. [score:5]
According to previous studies, MIR376 family members play a suppressive role in OS [18, 19]. [score:3]
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9
[+] score: 29
The 4.8-kb gigaloop is a putative structure formed by pairing of VCR and a complementary sequence (cVCR) Figure 2. Conserved sequences of stratum 1 (shared by Homo and Callorhinchus IGF1R 3'-UTRs): (a) the 3' end of the long IGF1R transcript; (b) a miR-7-3p target site that has been lost from the Pelodiscus sequence; (c) let-7-3p target site; (d) miR-186 target site; (e) The VCR with predicted binding sites for miR-376c, miR-675 (derived from the imprinted H19 RNA) and miR-16. [score:7]
The VCR contains a target site for miR-675 [13], a target site for the miR-16 family of microRNAs [24, 25] and a target site for miR-376c [26]. [score:7]
Either the miR-675 and miR-376 binding sites were targets for unidentified ancient microRNAs, perhaps still present in Pelodiscus and Callorhinchus, or the more recent imprinted microRNAs evolved to target sequences that were conserved for functions unrelated to binding by microRNAs. [score:5]
If the latter scenario is correct, then the VCR is likely to have been an original target of miR-675 and miR-376 which evolved to target its sequence. [score:5]
It is notable that miR-675 and miR-376 are both imprinted and maternally expressed [12, 27]. [score:3]
The miR-376 binding site occurs distal to the end of the short transcript. [score:1]
By contrast, miR-675 is known only from marsupial and eutherian mammals [35, 36] and miR-376 only from eutherian mammals [27]. [score:1]
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10
[+] score: 18
Of particular interest, up-regulated miRNAs miR-494 and miR-495 were predicted to target CTNND2, while up-regulated miR-376c and miR-409-3p were predicted to target NR2F2, which were both down-regulated in primary MB specimens relative to CD133+ NSCs (Table S4). [score:14]
In particular, several miRNAs mapping to 14q32, including miR-376c, miR-495 and miR-539, were identified as up-regulated in MB specimens defined by a neuronal differentiation signature (sub-type C as per [8]) [33]. [score:4]
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11
[+] score: 18
Modulation of pulmonary miRNAs targeting p53 (miR-138 and miR-376c) and apoptosis (miR-98 and miR-350) is consistent with the notion that AMPK is involved in the p53 -mediated cell cycle arrest and apoptosis 2. Several miRNAs upregulated in the lung of metformin -treated mice, including miR-30b, miR-138, miR-239a, miR-342, and miR-574, are involved in stress response and inflammation and target NF κB or Tlr9 (Toll-like receptor). [score:8]
In our in vivo study, the expression of miRNAs targeting Ras (let-7f, miR-135b, miR-143, miR-466h, miR-470, and miR-487b) was regulated in the lung of metformin -treated mice, along with another miRNA (miR-376c) playing an antioxidant role. [score:6]
In addition, metformin modulated the expression of a number of miRNAs (let-7f, miR-30b, miR-362, miR-376c, miR-466h, miR-490, and miR-574) involved in the regulation of the cell cycle, which is a crucial mechanism in the AMPK -mediated activity of this drug 42. [score:4]
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12
[+] score: 15
On the other hand, a number of down-regulated miRNAs, such as miR-378a-5p [19], miR-376c [16], and miR-195 [20], promote trophoblast cell proliferation, survival, and/or invasion. [score:4]
Similar to miR-378a-5p, miR-376c also promotes trophoblast cell proliferation and survival partially by regulating Nodal and TGF-β signaling as it represses the expression of activin receptor-like kinase 5 (ALK5) and ALK7, type I receptors for TGF-β and Nodal, respectively [16]. [score:4]
MicroRNA-376c induced trophoblast invasion and migration and explants outgrowth by targeting ALK7 and ALK5 to impair Nodal/TGF-β signaling [16]. [score:2]
Interestingly, the decrease in plasma miR-376c levels are found at 16–18 weeks of pregnancy, in a group of subjects who later developed PE, suggesting the possibility of using miR-376c as a predictive biomarker for PE [16]. [score:1]
Our recent studies show that plasma miR-376c levels are lower in PE patients than in control subjects. [score:1]
Our finding that placental miR-376c levels are higher in the third trimester than in the first trimester is conflicting with the qPCR array results reported by Morales-Prieto et al. [90]. [score:1]
Some miRNAs, such as miR-195 [20], miR-376c [16], and miR-378a-5p [19], have been reported to enhance trophoblast migration/invasion. [score:1]
In our recent studies, we found that miR-378a-5p levels were higher in first and second trimester than in third trimester placenta [19] while miR-376c levels were higher in second and third trimesters than that in the first trimester [16]. [score:1]
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13
[+] score: 12
miR-376c-3p and miR-342-3p were predicted to affect tau phosphorylation by directly targeting the 3′-UTR of PP2A. [score:4]
Considering a probe signal of over 100 as abundance, eleven of the 28 miRNAs (miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p) were shown to have targets that are tightly related to AD and could easily be detected. [score:3]
Several miRNAs derived from our microarray analysis targeted PTEN, such as miR-376c-3p, miR-342-3p, let-7f-5p, miR-10a-5p, miR-301b-3p, miR-98-5p, miR-1251-5p, and miR-34a-5p. [score:3]
For further analysis, we chose 11 evidently different miRNAs that were conserved between both human and mouse: miR-342-3p, miR-342-5p, miR-376c-3p, miR-301b-3p, let-7f-5p, miR-539-3p, miR-491-3p, miR-10a-5p, miR-98-5p, miR-652-5p, and miR-34a-5p. [score:1]
To our knowledge, this is the first study to identify the potential effects of miR-342-3p, miR-491-3p, miR-539-3p, miR-376c-3p, miR-10a-5p, and miR-652-5p in the progression of AD. [score:1]
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14
[+] score: 12
As shown in Figure 2, the serum levels of miR-17, miR-20a and miR-106a were significantly elevated in response to virus infection (p < 0.01), consistent with the results from the TaqMan Arrays, while the expression of miR-376c in serum samples of H7N9 patients was slightly higher than that in healthy controls (p < 0.05). [score:3]
Figure 4 ROC curve for a combination of miR-17, miR-20a, miR-106a and miR-376c was constructed. [score:1]
In summary, we, for the first time, provided an overview of host serum miRNA alterations in response to H7N9 virus infection, as well as identified the diagnostic ability of combined miR-17, miR-20a, miR-106a and miR-376c serum levels, thus promoting our understanding of this emerging virus pathogenesis. [score:1]
Finally, an important question remains to be answered: whether the serum levels of four miRNAs (miR-17, miR-20a, miR-106a and miR-376c) could be used for discriminating H7N9 virus from other types of viral infections with the same good performance. [score:1]
In contrast, the diagnostic capacity of miR-376c was relatively low for infection (AUC value: 0.622; 95% CI: 0.464–0.779) (Figure 3D). [score:1]
When the serum levels of these four miRNAs were subjected to combined analysis by multiple logistic regression, the generated ROC curve reflected a higher ability to differentiate patients with H7N9 virus infection from healthy controls (AUC value: 0.96; 95% CI: 0.917–1.000), demonstrating the diagnostic accuracy of miR-17, miR-20a, miR-106a and miR-376c as effective biomarkers in combination (Figure 4). [score:1]
Figure 2The serum levels of miR-17, miR-20a, miR-106a and miR-376c were determined by quantitative RT-PCR in individual healthy controls (n = 36) and patients (n = 21). [score:1]
MiR-17 (A), miR-20a (B) and miR-106a (C) showed a moderate discriminating efficiency with an AUC value more than 0.8, while miR-376c (D) exhibited a poor diagnostic ability with an AUC value of 0.622. [score:1]
Four miRNA molecules (miR-17, miR-20a, miR-106a and miR-376c) were selected for validation of the TaqMan Array data in a larger scale population by quantitative RT-PCR. [score:1]
Furthermore, miR-17, miR-20a, miR-106a and miR-376c used in this study for the diagnosis of H7N9 virus infection did not overlap with those for enterovirus and H1N1 virus infections, thus indicating high diagnostic specificity of these four miRNAs. [score:1]
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15
[+] score: 10
Other miRNAs from this paper: hsa-mir-376a-1, hsa-mir-376b, hsa-mir-376a-2
Thus, PRPS1 expression plays a role in fetal inner ear development, and mutations to the PRPS1 gene or to miRNA-376 may result in abnormal organ development. [score:6]
The transcript levels of PRPS1 are regulated by mir-376. [score:2]
PRPS1, transcriptionally regulated by microRNA-376 [5], codes for PRS-I, which catalyzes the synthesis of phosphoribosylpyrophosphate (PRPP) from adenosine triphosphate (ATP) and ribose-5-phophate (R5P) [4, 6]. [score:2]
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16
[+] score: 10
0014416.g004 Figure 4 (A) of stably expressing miR-376a, miR376abc (a polycistronic cluster of miR-376a, miR-376b and miR-376c), miR-299-5p or miR -negative and 10-87 LP cells; (B) with stably expressing miR-376a, miR-376abc, miR-299-5p or miR -negative 10-87 HP cells. [score:5]
Indeed, the overexpression of miR-376a and the polycistronic cluster of miR-376a, miR-376b and miR-376c in non-invasive 10-87 LP cells were able to recapitulate the migration and invasion phenotypes of 10-87 HP cells. [score:3]
An expression plasmid for the polycistronic gene cluster for miR-376a, miR-376b and miR-376c was generated by amplifying 200 bp up-stream and 200 bp down-stream of the genes (termed as miR-376abc) in VERO cell DNA using primers 5′-CCCTCGACGAGAGTGATGGAAGGTGAATC-3′ and 5′-CCAGATCTATACTGAGAACACAGCCTTGT-3′. [score:2]
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17
[+] score: 9
Overall, 31% and 50% of the miR-376c and 86% and 50% of the miR-376a were expressed as the edited form in HCC and ANL, respectively. [score:3]
A recent study has reported tissue-specific editing of miR-376 cluster members and the expression of edited mature miR-376 RNAs in certain tissues [20]. [score:3]
For miR-376c, miR-376a, miR-34a, miR-503, miR-21, and miR-122, the RNA modifications were detected using both methods, and the possibility of a single nucleotide polymorphism at any of the RNA editing sites was excluded by comparison with the public database OncoDb HCC. [score:1]
First, in miR-376c and miR-376a, members of miR-376 cluster, specific adenosine (A) residues in the seed sequence (+6 site) were detected as guanosine (G) in the sequencing chromatogram, which suggests adenosine to inosine (I) editing [20]. [score:1]
Modified miR-376c, miR-376a, miR-34b*, and miR-503 are detected by RT-PCR and conventional cloning. [score:1]
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18
[+] score: 9
In a human intrahepatic CC cell line, downregulation of miR-376c, which is suggested to function as a tumor suppressor, accelerated EGF -dependent migration through its direct target growth factor receptor bound protein 2 (GRB2) [233]. [score:9]
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19
[+] score: 9
Antagomir -mediated inhibition of miR-21-3p and miR-223 (increased expression following bacterial infection), or miR-376c (decreased expression), and miR-21 (control, no change in expression) had no effects on NTHi clearance by neutrophils in vitro (S11 Fig). [score:9]
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20
[+] score: 8
Zhu et al. reported that miR-152 could potentially controls migration and invasion by targeting TGF-α in prostate cancer cell lines [29]; Jin et al. reported that miR-376c could inhibit cell proliferation and invasion by targeting TGF-α in osteosarcoma [30]; Qin et al. reported that miR-124 may regulates TGF-α -induced EMT in human prostate cancer cells [31]. [score:8]
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21
[+] score: 8
With an exceedingly stringent Sidak correction, only 4 differentially regulated miRs were identified; miR-200a, 345, 376c, and 888. miR345 is a methylation-sensitive miR (down-regulated) which is involved in cell proliferation and invasion in colorectal cancer [47], while miR-376c (here up-regulated) enhances ovarian cancer cell survival and has been implicated in chemoresistance [48]. [score:8]
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22
[+] score: 8
Other miRNAs from this paper: hsa-mir-127, hsa-mir-154, hsa-mir-494, hsa-mir-495, hsa-mir-496
Based on the qRT-PCR results, the hESCs with higher MEG3 and MEG8 expression were classified as MEG3-ON hESCs, in which several miRNAs from this locus, miR-127-3p, miR-154, miR-376c, miR-494, miR-495, and miR-496, were also abundantly expressed (Figure  1B). [score:5]
The UPL probe system (Roche) was used to detect the expression of miRNAs, including miR-127-3p, miR-376c, miR-494, miR-495, miR-496, and miR-154. [score:3]
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23
[+] score: 7
Recent studies indicate that during human pancreatic development miR-7, miR-9, miR-375 and miR-376 are specific islet microRNAs expressed at high levels [18, 19]. [score:4]
Please note that even though in some cases the group III colorgram suggests a change of expression throughout the gestational stages (e. g miR-376, miR-378, etc), these were found to be not statistically significant. [score:3]
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24
[+] score: 7
These included predicted binding of spliced genes to three forms of hsa-miR-376 (a–c forms), hsa-mir-544 targeted at the same spliced gene (ITGAL) and the inflammation-related hsa-mir-150 [87] predicted to target the disease spliced gene FGD4. [score:7]
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25
[+] score: 7
Kawahara and colleagues demonstrated that A-to-I editing of pri-miR-376 results in the redirection of its silencing effects to a different set of target mRNAs. [score:4]
The miR-376 is edited by ADAR2 within its “seed” sequence (+4 site), an essential region for RNA duplex formation with the complementary target mRNA [95]. [score:3]
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26
[+] score: 7
Importantly, in the case of mir-376a-5p, mir-376b-5p, mir-376a-3p and mir-376-3p the edited nucleoside resides in the seed region, which is instrumental in targeting the miRNA to its target and could therefore lead to an altered target spectrum. [score:7]
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27
[+] score: 7
Indeed, concomitantly with weight loss and improved AT inflammation (Additional file 2: Table S2), current data pointed decreased AT expression of miRNAs which detection inside isolated cells (for example, miR-146b, miR-376c, miR-411) and/or in the SN (miR-221, miR-222, miR-155, miR-223, miR-19a/b) rose in differentiated adipocytes upon inflammatory stimuli (Table  2). [score:3]
On the other hand, the expression of ‘miRNokines’ such as miR-146b, miR-376c, miR-411, and miR-19a by inflamed adipocytes/obese AT may hint into functional activities beyond adiposity, such as recruitment of immune cells [25], or modulation of insulin-secreting cells [26]. [score:3]
Indeed, some miRNAs became undetectable (miR-1274B, miR-572, and miR-766), while others appeared de novo in cells (miR-140-5p, miR-222*, miR-376c, miR-411, and miR-146a) and their SNs (miR-146a, miR-146b, miR-19a, miR-223*, miR-425, and miR-9*) upon MCM -induced inflammation (Figure  2). [score:1]
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28
[+] score: 7
The upregulated miRNAs included miR-132-3p, miR-604, miR-186-5p, miR-29b-3p, miR-125b-5p, miR-376c-3p, and miR-30b-5p, where the only downregulated miRNA was miR-423-3p (Table 1). [score:7]
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29
[+] score: 6
Biological support to this mode was given by Nachmani et al. [14] showing that hcmv-miR-UL112-1 and hsa-miR-376, which have distinct target sites on MICB mRNA, cooperate within infected cells to down-regulate MICB. [score:6]
[1 to 20 of 1 sentences]
30
[+] score: 6
The discovery of dysregulated miRNAs, e. g., miR-210, miR-376c, and miR-455, and their gene-regulatory roles in placental development has provided a new avenue for elucidating the underlying mechanisms of pregnancy-specific diseases, such as PE 17– 19. [score:6]
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31
[+] score: 6
Haller et al. revealed the deregulation of miRNA-329, miR-370, miR-376c and miR409 expression based on the location of the tumor in gastrointestinal stromal tumors (GISTs); higher expression occurred in intestinal compared to gastric tumors [46]. [score:5]
Indeed, it has even been proposed that miR-376c can promote cell proliferation and invasion [47, 48]. [score:1]
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32
[+] score: 6
The canonical version of miR-376 and its seed-altered isomiR were shown to have highly distinct target sets [29], highlighting the biological importance of 5′-isomiRs. [score:3]
Perhaps the best-studied example of this phenomenon is the A-to-I editing of the miR-376 primary transcript leading to the expression of a 5′-isomiR of miR-376 with a modified seed [29]. [score:3]
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33
[+] score: 5
e. m. value of hsa-miR-137, hsa-miR-376c-3p, hsa-miR-203a-3p and hsa-miR-146a-5p relative expression level in two series of biological replicates from the first microfluidics arrays (five control and five FD hOE-MSCs) and the second arrays (four healthy control and four FD hOE-MSCs), respectively normalized by hsa-miR-320a (for both hsa-miR-137 and hsa-miR-376c-3p), hsa-miR-330-3p and hsa-miR-324-5p. [score:3]
We validated a significant underexpression in FD compared to control hOE-MSCs for all four miRNAs: miR-137, miR-376c-3p, miR-203a-3p and miR-146a-5p (Fig.  2). [score:2]
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34
[+] score: 5
In a separate study, the increase of miR-376c level in ovarian cancer cells was found to inhibit cisplatin induced cell death [100]. [score:3]
Nine of those 11 miRNAs including miR-433, miR-127, miR-381, miR-377, miR-299-3p, miR-409-3p, miR-154, miR-382, and miR-376c are associated with OS. [score:1]
Besides that miR-376c has been shown to be associated with nodal metastasis in gastric cancer and miR-494 is significantly correlated with gastric cancer stage. [score:1]
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35
[+] score: 5
Altered expression of miRNA-221, miRNA-744, and miRNA-376c significantly give a positive identification of the disease (Sandoval-Borquez et al., 2015). [score:5]
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36
[+] score: 5
Real-time quantitative PCR allowed analysis of six miRNAs that were differentially expressed in the experimental groups: miR-31-3p, miR-134, miR-136-3p, miR-376C-3p, miR-494, and miR-424-5p (Table 6). [score:3]
mRNA and microRNA oligoarray data were confirmed by qRT-PCR for five mRNAs (SMURF2, NOTCH1, PHOSPHO1, COL24A1, and FGF1) and six microRNAs (miR-31-3p, miR-134, miR-136-3p, miR-376c-3p, miR-424-5p, and miR-494). [score:1]
These miRNAs are associated with several functions like apoptosis (miR-134 and miR-494), bone mineralization (miR-31-3p, miR-136-3p, miR-376C-3p, and miR-424-5p), and cell growth and proliferation (miR-134) (http://geneontology. [score:1]
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37
[+] score: 5
While expression of miR-136, miR-376a and miR-377 did not significantly change during treatment, expression of miR-376c and miR-127-3p was significantly increased by Aza treatment and was further elevated by the combined treatment with Aza and PBA. [score:5]
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38
[+] score: 5
For example, the miRNA couple composed of hsa-let-7g and hsa-miR-376c has most targets in common (14 mutual target genes: AMMECR1L, CYP26A1, ZFYVE26, MUC7, FUS, TMEM38B, CWH43, CWH43, LIN28B, ZNF823, DVL3, SRGN, INPP5A, HDAC8). [score:5]
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39
[+] score: 4
In this follow up study, we selected nine miRNA candidates (miR-125-3p, miR-320c, miR-320d, miR-9-1, miR-139, miR-125a-5p, miR-4792, miR-376, miR-543, miRNA-381) for validation in the independently recruited patients with early-stage (I, II) colon cancer. [score:1]
MiR-9-1, miR-125a-3p, miR-125a-5p, miR-320c, miR-320d, miR-4792, miR-376, miR-139, miR-543, and miR-381(MS00010752, MS00008554, MS00003423, MS00041867, MS00031710, MS00045087, MS00007392, MS00003493, MS00010080, MS00004116, QIAGEN, Valencia, CA) were selected for downstream validation. [score:1]
In this study, we selected miR-9-1, miR-125a-3p, miR-125a-5p, miR-320c, miR-4792, miR-376, miR-543, and miR-381 as diagnostic candidates for validation. [score:1]
For early diagnosis of CRC, A panel of four-miRNA signature consisting of miR-23a-3p, miR-27a-3p, miR-142-5p and miR-376c-3p was established with AUC of 0.917 [23]. [score:1]
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[+] score: 4
According to the study conducted by Mo and colleagues, human ESCs with low MEG3 expression level (designated as MEG3-OFF) also showed significantly low expressions of DLK1-DIO3 locus-derived noncoding RNAs, including MEG8, miR-127, miR-376, miR-494, miR-495, miR-496, and miR-154, compared to its counterpart MEG3-ON [68]. [score:4]
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[+] score: 4
Among them, the expression patterns of miR-221, miR-744 and miR-376c in serum could be used as biomarkers to distinguish gastric cancer patients from healthy individual (Ref. [score:3]
Several miRNAs circulating in blood of gastric cancer patients can be applied as diagnosis biomarkers, including let-7a, miR-1, miR-17-5p, miR-21, miR-20a, miR-27a, miR-34, miR-106a/b, miR-196a, miR-199a-3p, miR-218, miR-221, miR-223, miR-370, miR-376c, miR-378, miR-421, miR-423-5p, miR-451 and miR-486 (Refs 64, 76, 111, 112, 113, 114, 115, 116, 117). [score:1]
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[+] score: 4
The analysis of randomly-chosen miRNAs from clusters 1 and 2 (miR-654-3p, mir-369-3p, miR-495, miR-370-5p, miR-127-5p and miR-376c-3p) in tumor cell lines confirmed their downregulation (Figure 1d). [score:4]
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43
[+] score: 4
MiR-8 [20], miR152 [21], miR124 [22] and miR-376c [23] have been reported to regulate the expression of TGFα. [score:4]
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44
[+] score: 4
Previous studies have provided evidence for the important roles of deregulated expression of miRNAs in the pathogenesis of CC, including miR-29, miR-122, miR-124, miR-145, miR-146a, miR-200c, miR-370, miR-373, miR-376c and miR-494 [30– 36]. [score:4]
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[+] score: 4
Fu et al.  reported in 2013 that miR-376c levels were downregulated in both placental and plasma samples at 16–18 weeks of pregnancy in 11 women who later developed PE, suggesting the possibility of using miR-376c as a predictive biomarker for PE [36]. [score:4]
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[+] score: 4
22 hsa-miR-224 1.43 hsa-miR-26a −1.26 hsa-miR-29a −1.21 hsa-miR-376c 1.26 hsa-miR-424 −1.35 hsa-miR-455-3p 1.48 hsa-miR-99a † 1.21 Italic: down-regulated in fat cells from obese. [score:4]
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[+] score: 4
As for noncoding RNA, Zhang et al. demonstrated that miR-376c-3p negatively regulated the expression of LINC00152 in colorectal cancer cells, restricting cell viability and stimulating cell apoptosis [24]. [score:4]
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[+] score: 3
For example, miR-144, miR-937, miR-376, miR-519, and miR-548A-3P are shown to regulate a number of mRNAs, and HCK, NFKBIE, IL6, SHMT2, and MCM4 are regulated by several miRNAs. [score:3]
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49
[+] score: 3
Racial differences in human platelet PAR4 reactivity reflect expression of PCTP and miR-376c. [score:3]
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50
[+] 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-15a, hsa-mir-16-1, hsa-mir-17, hsa-mir-18a, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-27a, hsa-mir-29a, hsa-mir-30a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-101-1, hsa-mir-106a, hsa-mir-107, hsa-mir-16-2, hsa-mir-192, hsa-mir-196a-1, hsa-mir-199a-1, hsa-mir-129-1, hsa-mir-148a, hsa-mir-10b, hsa-mir-34a, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-196a-2, hsa-mir-199a-2, hsa-mir-203a, hsa-mir-210, hsa-mir-212, hsa-mir-214, hsa-mir-215, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-mir-223, hsa-mir-200b, hsa-let-7g, hsa-let-7i, hsa-mir-1-2, hsa-mir-15b, hsa-mir-27b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-130a, hsa-mir-141, hsa-mir-142, hsa-mir-143, hsa-mir-145, hsa-mir-153-1, hsa-mir-153-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-129-2, hsa-mir-146a, hsa-mir-150, hsa-mir-185, hsa-mir-195, hsa-mir-206, hsa-mir-200c, hsa-mir-1-1, hsa-mir-155, hsa-mir-181b-2, hsa-mir-106b, hsa-mir-29c, hsa-mir-200a, hsa-mir-101-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-130b, hsa-mir-375, hsa-mir-378a, hsa-mir-148b, hsa-mir-338, hsa-mir-335, hsa-mir-423, hsa-mir-20b, hsa-mir-429, hsa-mir-449a, hsa-mir-433, hsa-mir-451a, hsa-mir-193b, hsa-mir-520d, hsa-mir-503, hsa-mir-92b, hsa-mir-610, hsa-mir-630, hsa-mir-650, hsa-mir-449b, hsa-mir-421, hsa-mir-449c, hsa-mir-378d-2, hsa-mir-744, hsa-mir-1207, hsa-mir-1266, hsa-mir-378b, hsa-mir-378c, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-4512, hsa-mir-378i, hsa-mir-203b, hsa-mir-451b, hsa-mir-378j
Of these, miR-17-5p, miR-18a, miR-20a, miR-200c, miR-21, miR-218, miR-221, miR-222, miR-25, miR-27a, miR-376c, and miR-744 were found to be significantly elevated in GC patients, and their expression was significantly reduced after surgery [26, 27, 54, 68, 71, 80, 81, 155, 187, 192, 193, 195, 196, 198, 199, 200, 201, 202, 203, 204, 205]. [score:3]
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[+] score: 3
It should be noted that the differential expression between grades I and II observed in deep sequencing in a few miRNAs (miR-21, miR-34a, miR-376, miR-451 and miR-99a) were not verified in RT-qPCR (Table 2 and Table 3). [score:3]
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[+] score: 3
Overexpression of mir-378a or miR-376c significantly enhanced proliferation, migration and invasion of the extravillous trophoblast (EVT)-like cell line HTR8/SVneo, and both mimetics promoted outgrowth of primary EVT from placental explants 37, 38. [score:3]
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53
[+] score: 3
In AGS [GR] cells treated with 10nM G17 compared with untreated controls, miScript miRNA PCR arrays showed 3 miRNAs that increased and 3 miRNAs that decreased in expression beyond the 2-fold threshold, with only miR-222 and miR-376c proving significant. [score:2]
However, only miR-376c and miR-222 proved significant with fold changes of 5.2 (P < 0.01) and 2.3 (P < 0.0001) respectively. [score:1]
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[+] score: 3
miRNAs [a]Presence in samples [b]Median editing (in %) Seed editing event Position in precursor Target Prediction [c]Overlap (%) Before/After editing hsa-mir-598-3p 6/5/0 0.49/0.34/0 Yes 62 11/9 0 (0) hsa-mir-376a-1-5p 6/6/0 11.24/8.43/0 Yes 9 131/166 4 (3.05) hsa-mir-337-3p* 4/1/0 4.21/−/0 Yes 66 146/197 11 (7.53) hsa-mir-376c-3p 6/5/2 3.72/1.9/− Yes 48 156/192 11 (7.05)hsa-mir-1301-3p [#,*] 6/6/2 7.59/3.94/− Yes 52 230/7 2 (0.87) hsa-mir-421 6/6/3 1.40/0.61/0.57 Yes 54 271/4 1 (0.37) hsa-mir-99b-3p* 6/6/2 3.61/1.65/− Yes 47 33/21 0 (0) hsa-mir-641-5p 6/6/3 5.62/7.08/3.35 Yes 18 355/128 11 (3.1) hsa-let-7e-3p* 4/0/0 2.09/0/0 Yes 57 5/3 0 (0)hsa-mir-1251-5p [#,*] 4/4/0 11.98/11.87/0 Yes 10 58/305 4 (6.9)hsa-mir-381-3p [#] 6/6/5 6.87/7.15/3.07 Yes 52 638/302 48 (7.52) hsa-mir-411-5p 6/6/5 27. [score:3]
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However, in rare cases, such as mir-376, RNA editing causes base substitution in the seed sequence and generates edited mature miRNAs with unique target genes and functions different from those of the unedited miRNAs (Kawahara et al., 2007). [score:3]
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Notably, microRNAs hsa-miR-127-5p, hsa-miR-370 and hsa-miR-376 had been shown to be highly and specifically expressed in islets of developing and adult human pancreas [53, 54]. [score:3]
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[+] score: 2
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-19b-2, hsa-mir-20a, hsa-mir-21, hsa-mir-22, hsa-mir-26a-1, hsa-mir-29a, hsa-mir-92a-1, hsa-mir-92a-2, hsa-mir-93, hsa-mir-99a, hsa-mir-101-1, hsa-mir-29b-1, hsa-mir-29b-2, hsa-mir-106a, hsa-mir-16-2, hsa-mir-197, hsa-mir-199a-1, hsa-mir-148a, hsa-mir-30c-2, hsa-mir-10a, hsa-mir-34a, hsa-mir-182, hsa-mir-199a-2, hsa-mir-205, hsa-mir-210, hsa-mir-221, hsa-mir-223, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-122, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-125b-1, hsa-mir-132, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-140, hsa-mir-142, hsa-mir-143, hsa-mir-125b-2, hsa-mir-134, hsa-mir-146a, hsa-mir-150, hsa-mir-206, hsa-mir-155, hsa-mir-29c, hsa-mir-30c-1, hsa-mir-101-2, hsa-mir-130b, hsa-mir-26a-2, hsa-mir-361, hsa-mir-362, hsa-mir-363, hsa-mir-371a, hsa-mir-375, hsa-mir-376a-1, hsa-mir-378a, hsa-mir-342, hsa-mir-151a, hsa-mir-324, hsa-mir-335, hsa-mir-345, hsa-mir-423, hsa-mir-483, hsa-mir-486-1, hsa-mir-146b, hsa-mir-202, hsa-mir-432, hsa-mir-494, hsa-mir-495, hsa-mir-193b, hsa-mir-497, hsa-mir-455, hsa-mir-545, hsa-mir-376a-2, hsa-mir-487b, hsa-mir-551a, hsa-mir-571, hsa-mir-574, hsa-mir-576, hsa-mir-606, hsa-mir-628, hsa-mir-629, hsa-mir-411, hsa-mir-671, hsa-mir-320b-1, hsa-mir-320c-1, hsa-mir-320b-2, hsa-mir-378d-2, hsa-mir-889, hsa-mir-876, hsa-mir-744, hsa-mir-885, hsa-mir-920, hsa-mir-937, hsa-mir-297, hsa-mir-1233-1, hsa-mir-1260a, hsa-mir-664a, hsa-mir-320c-2, hsa-mir-2861, hsa-mir-378b, hsa-mir-1260b, hsa-mir-378c, hsa-mir-1233-2, hsa-mir-378d-1, hsa-mir-378e, hsa-mir-378f, hsa-mir-378g, hsa-mir-378h, hsa-mir-378i, hsa-mir-664b, hsa-mir-378j, hsa-mir-486-2
Circulating serum miR-17, miR-20a, miR-106a, and miR-376c were significantly increased in expression for patients compared to healthy individuals (220). [score:2]
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58
[+] score: 2
Formosa A, Markert EK, Lena AM, Italiano D, Finazzi-Agro E, Levine AJ, et al. s, miR-154, miR-299-5p, miR-376a, miR-376c, miR-377, miR-381, miR-487b, miR-485-3p, miR-495 and miR-654-3p, mapped to the 14q32.31 locus, regulate proliferation, apoptosis, migration and invasion in metastatic prostate cancer cells. [score:2]
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[+] score: 2
The first one, previously published [18], is located within the seed region of mir-376c (Additional file 2: Figure S3). [score:1]
The editing site is located in the seed region of mir376c. [score:1]
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60
[+] score: 2
In addition, a number of other miRNAs, including miR-30d, let-7e, miR-21, miR-9, and miR-376, are also implicated in human pancreatic islet differentiation and development [25, 26, 27]. [score:2]
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61
[+] score: 2
B) ROC Curve for miR-523, miR-218, miR-142-3p,miR-27a,miR-376c,miR-374. [score:1]
miRNA ΔΔCT(mean) p-value miR-374 -0.4458 0.454 miR-142-3p -0.4136 0.4322 miR-523 -0.5518 0.3424 miR-374-5p -0.2611 0.6425 miR-376c -0.4312 0.5867 miR-27a -0.3863 0.4776 miR-520d-5p -0.3081 0.7506 miR-122 -0.0856 0.9251 miR-485-3p -0.2611 0.6392 miR-21 -0.3976 0.5261 miR-218 -1.332 0.1659 miR-374 -0.4458 0.454 Comparison of mean ΔΔCT’s for various plasma miRNA from plasma samples drawn from the same 7 individuals on the same day 12 hours apart. [score:1]
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62
[+] score: 2
Regulation of Human UGT2B15 and UGT2B17 by miR-376c in Prostate Cancer Cell Lines. [score:2]
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63
[+] score: 2
Congruent with previous studies, A to G changes occurred in >60% of the reads for members of the miR-376 family (miR-376a, b, and c) at nucleotide position six of the mature miRNA sequence (Table 1, Fig. S3A) [36]. [score:1]
Furthermore, several of these miRNA variants (miR-376 family members, miR-411, miR-379, and miR-320a) have previously been described in deep sequencing studies performed on human brain [36], [37], and therefore, are not specific to glioblastoma. [score:1]
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64
[+] score: 2
Not all miRNA editing events are ancient: we found six cases of miRNA editing (miR-376a-1, miR-376b, miR-376c, miR-379, miR-381 and miR-411) that were limited to placental mammals and that therefore represent evolutionary novelties (Figure  1). [score:1]
Editing of miR-376b, miR-376c, miR-379, miR-381, miR-411 and miR-497 was significantly correlated with age in both species, demonstrating that the age-related increase of editing frequencies at specific sites is conserved between species (Figure  4B). [score:1]
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65
[+] score: 2
From the remaining deregulated miRNAs, the most significant were hsa-miR-23/27 cluster and hsa-let-7, hsa-miR-30, and hsa-miR-376 families. [score:2]
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66
[+] score: 2
In prostate cancer cells, miR-376 was shown to be involved in regulation of proliferation, apoptosis, migration and cell invasion [43]. [score:2]
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67
[+] score: 2
Other miRNAs from this paper: hsa-mir-152, hsa-mir-193a
Linc00152 was negatively regulated by miR-376c-3p, restricting cell viability, and stimulates cell apoptosis in colorectal cancer [36]. [score:2]
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68
[+] score: 1
For the two other novel bat miRNAs within this cluster (pal-can-411 and pal-can-252), the mature sequences produced non-identical BLAST hits to miR-376 and miR-377, respectively, however the star sequences were 100% identical to miR-376 and miR-377 star sequences, respectively. [score:1]
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69
[+] score: 1
For example, Labialle et al. reports that part of Dlk1-Dio3 mat region (the miR-379 / miR-410 cluster), which included five of the candidate NAFLD miRNAs (miR-376c, -379, -409, -411, and -495), affects energy metabolism including gluconeogenesis in neonatal mouse [35]; selective ablation of the miR-379 / miR-410 cluster causes lethal blood hypoglycemia. [score:1]
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70
[+] 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-15a, hsa-mir-17, hsa-mir-21, hsa-mir-29a, hsa-mir-96, mmu-let-7g, mmu-let-7i, mmu-mir-124-3, mmu-mir-140, mmu-mir-181a-2, mmu-mir-182, mmu-mir-183, mmu-mir-194-1, mmu-mir-200b, hsa-mir-34a, hsa-mir-181a-2, hsa-mir-181b-1, hsa-mir-181c, hsa-mir-182, hsa-mir-183, hsa-mir-181a-1, hsa-mir-200b, mmu-mir-34c, mmu-mir-34b, mmu-let-7d, hsa-let-7g, hsa-let-7i, hsa-mir-124-1, hsa-mir-124-2, hsa-mir-124-3, hsa-mir-140, hsa-mir-194-1, 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-21a, mmu-mir-29a, mmu-mir-96, mmu-mir-34a, mmu-mir-135b, hsa-mir-200c, hsa-mir-181b-2, mmu-mir-17, mmu-mir-200c, mmu-mir-181a-1, mmu-mir-124-1, mmu-mir-124-2, mmu-mir-181b-1, mmu-mir-181c, hsa-mir-194-2, mmu-mir-194-2, hsa-mir-34b, hsa-mir-34c, hsa-mir-376a-1, mmu-mir-376a, hsa-mir-135b, mmu-mir-181b-2, mmu-mir-376b, dre-mir-34a, dre-mir-181b-1, dre-mir-181b-2, dre-mir-182, dre-mir-183, dre-mir-181a-1, dre-let-7a-1, dre-let-7a-2, dre-let-7a-3, dre-let-7a-4, dre-let-7a-5, dre-let-7a-6, dre-let-7b, dre-let-7c-1, dre-let-7c-2, dre-let-7d-1, dre-let-7d-2, dre-let-7e, dre-let-7f, dre-let-7g-1, dre-let-7g-2, dre-let-7h, dre-let-7i, dre-mir-15a-1, dre-mir-15a-2, dre-mir-17a-1, dre-mir-17a-2, dre-mir-21-1, dre-mir-21-2, dre-mir-29a, dre-mir-96, dre-mir-124-1, dre-mir-124-2, dre-mir-124-3, dre-mir-124-4, dre-mir-124-5, dre-mir-124-6, dre-mir-140, dre-mir-181c, dre-mir-194a, dre-mir-194b, dre-mir-200b, dre-mir-200c, hsa-mir-376b, hsa-mir-181d, hsa-mir-507, dre-let-7j, dre-mir-135b, dre-mir-181a-2, hsa-mir-376a-2, mmu-mir-376c, dre-mir-34b, dre-mir-34c, mmu-mir-181d, mmu-mir-21b, mmu-let-7j, mmu-mir-21c, mmu-let-7k, dre-mir-181a-4, dre-mir-181a-3, dre-mir-181a-5, dre-mir-181b-3, dre-mir-181d, mmu-mir-124b
Analysis of miR-376 RNA cluster members in the mouse inner ear. [score:1]
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71
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Another study delineated miR-221, miR-376c, and miR-744 as markers for GC detection, which were capable of identifying GC even 5 years prior to clinical diagnosis [28]. [score:1]
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72
[+] score: 1
047  hsa-miR-376c 2.74. [score:1]
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73
[+] score: 1
73(12) hsa-miR-377* 14q32.2 −2.72 hsa-miR-7 15q25.3/19p13.3/9q21.32 −2.72(12, 14) hsa-miR-124 20p23.1/8q12.3/8p23.1 −2.71(12, 14, 29, 48, 49) hsa-miR-323-5p 14q32.31 −2.69(12) hsa-miR-873 9p21.1 −2.65 hsa-miR-129* 11p11.2/7q32.1 −2.63 hsa-miR-338-5p 17q25.3 −2.61(14) hsa-miR-409-5p 14q32.2 −2.61 hsa-miR-874 5q31.2 −2.46 hsa-miR-495 14q32.2 −2.46(52) hsa-miR-885-5p 3p25.3 −2.45 hsa-miR-376c 14q32.2 −2.43(52) hsa-miR-299-5p 14q32.2 −2.41 hsa-miR-539 14q32. [score:1]
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Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-mir-18a, hsa-mir-21, hsa-mir-23a, hsa-mir-26a-1, hsa-mir-30a, hsa-mir-99a, hsa-mir-103a-2, hsa-mir-103a-1, mmu-mir-1a-1, mmu-mir-23b, mmu-mir-30a, mmu-mir-99a, mmu-mir-126a, mmu-mir-9-2, mmu-mir-133a-1, mmu-mir-138-2, hsa-mir-192, mmu-mir-204, mmu-mir-122, hsa-mir-204, hsa-mir-1-2, hsa-mir-23b, hsa-mir-122, hsa-mir-133a-1, hsa-mir-133a-2, hsa-mir-138-2, hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-126, hsa-mir-138-1, mmu-mir-192, mmu-let-7a-1, mmu-let-7a-2, mmu-mir-18a, mmu-mir-21a, mmu-mir-23a, mmu-mir-26a-1, mmu-mir-103-1, mmu-mir-103-2, hsa-mir-1-1, mmu-mir-1a-2, mmu-mir-26a-2, mmu-mir-9-1, mmu-mir-9-3, mmu-mir-138-1, hsa-mir-26a-2, hsa-mir-381, mmu-mir-381, mmu-mir-133a-2, rno-let-7a-1, rno-let-7a-2, rno-mir-9a-1, rno-mir-9a-3, rno-mir-9a-2, rno-mir-18a, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-26a, rno-mir-30a, rno-mir-99a, rno-mir-103-2, rno-mir-103-1, rno-mir-122, rno-mir-126a, rno-mir-133a, rno-mir-138-2, rno-mir-138-1, rno-mir-192, rno-mir-204, mmu-mir-411, hsa-mir-451a, mmu-mir-451a, rno-mir-451, hsa-mir-193b, rno-mir-1, mmu-mir-376c, rno-mir-376c, rno-mir-381, hsa-mir-574, hsa-mir-652, hsa-mir-411, bta-mir-26a-2, bta-mir-103-1, bta-mir-16b, bta-mir-18a, bta-mir-21, bta-mir-99a, bta-mir-126, mmu-mir-652, bta-mir-138-2, bta-mir-192, bta-mir-23a, bta-mir-30a, bta-let-7a-1, bta-mir-122, bta-mir-23b, bta-let-7a-2, bta-let-7a-3, bta-mir-103-2, bta-mir-204, mmu-mir-193b, mmu-mir-574, rno-mir-411, rno-mir-652, mmu-mir-1b, hsa-mir-103b-1, hsa-mir-103b-2, bta-mir-1-2, bta-mir-1-1, bta-mir-133a-2, bta-mir-133a-1, bta-mir-138-1, bta-mir-193b, bta-mir-26a-1, bta-mir-381, bta-mir-411a, bta-mir-451, bta-mir-9-1, bta-mir-9-2, bta-mir-376c, bta-mir-1388, rno-mir-9b-3, rno-mir-9b-1, rno-mir-126b, rno-mir-9b-2, hsa-mir-451b, bta-mir-574, bta-mir-652, mmu-mir-21b, mmu-mir-21c, mmu-mir-451b, bta-mir-411b, bta-mir-411c, mmu-mir-126b, rno-mir-193b, mmu-mir-9b-2, mmu-mir-9b-1, mmu-mir-9b-3
A-to-G transitions potentially caused by A-to-I editing were mainly identified in miR-99a and miR-376c (Figure 2), which have been reported to undergo A-to-I editing in human and mouse, respectively [22, 23]. [score:1]
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The fine-grained structure of these loci has some species-specific aspects, as illustrated by Figures 2 and 3. The figures show all the validated miRNAs in these regions, including those with suboptimal prediction scores from the Additional files 7, 8, and 9. We find that some miRNAs that are related in sequence, and have presumably arisen by duplication (such as the mir-368/mir-376-related sequences) have different numbers of copies in rodents and human. [score:1]
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For examples, some miRNAs were identified to be involved in ICC cell growth and apoptosis (miR-31) [21], migration or invasion (miR-376c and miR-214) [22, 23], metastasis [24], and epithelial to mesenchymal transition (EMT) (miR-200c and miR-204) [19, 25]. [score:1]
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A recent computational analysis exploring the potential cross-talk between RBPs, such as PUM proteins, and miRNA -mediated repression of human mRNAs identified a specific group of miRNA (miR-30-abcde/385-5p, miR-144, miR-376c, miR-300, miR-101, miR-221/222, and miR-410) binding sites overrepresented near PUM recognition sites in the 3'-UTR, suggesting strong cooperation to control the decay of these mRNAs [22]. [score:1]
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We also choose to include seven miRNAs (mir-370, mir-337-5p, mir-376c, mir-377, mir-1247, mir-758 and mir-300) that are located on the q arm of chromosome 14, which has been found to be aberrant and implicated in many types of cancer [24]. [score:1]
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In contrary, miR-378a-5p, miR-376c, and miR-21 have been shown to enhance trophoblast proliferation and invasion via modulating the nodal signaling pathway (42– 44). [score:1]
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We checked the reference suggested by the reviewer and found that they have talked about only one family within the cluster of miR-376 (miR-376a, -b or-c). [score:1]
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