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18 publications mentioning hsa-mir-770

Open access articles that are associated with the species Homo sapiens and mention the gene name mir-770. Click the [+] symbols to view sentences that include the gene name, or the word cloud on the right for a summary.

[+] score: 272
Other miRNAs from this paper: hsa-mir-9-1, hsa-mir-9-2, hsa-mir-9-3, hsa-mir-136
In OVC patients with IR to cisplatin, miR-770-5p is downregulated and does not suppress ERCC2 expression; ERCC2 is thus overexpressed in OVC cells and activates excision repair of DNA damaged by cisplatin, ultimately accelerating tumor cell growth (B) Conversely, in OVC patients with CR to cisplatin, miR-770-5p is upregulated and strongly suppresses ERCC2 expression in tumor cells; this reduces ERCC2 -induced DNA damage repair, allowing cisplatin to damage DNA and ultimately activating tumor cell apoptosis (C) ERCC2 = excision repair cross-complementing rodent repair deficiency, group 2; IR = incomplete response; CR = complete response. [score:17]
Upregulation of miR-770-5p and downregulation of ERCC2 inhibits the repair of cisplatin -induced DNA-damage in vitro. [score:9]
Upregulation of miR-770-5p and downregulation of ERCC2 inhibits the repair of cisplatin -induced DNA-damage in vitroCisplatin and other platinum -based cancer drugs destroy tumor cells by binding to DNA strands, interfering with DNA replication, and forming cisplatin-DNA adducts; chemosensitivity results from the inability to repair this DNA damage. [score:9]
Together, these findings suggest that miR-770-5p might directly target ERCC2, the downregulation of which increases cisplatin chemosensitivity in OVC. [score:7]
First, miR-770-5p and ERCC2 expression were analyzed in CR and IR patients using qRT-PCR; miR-770-5p expression was negatively correlated with ERCC2 expression in both groups (Figure 4B). [score:7]
siRNA -mediated silencing of ERCC2 reversed the inhibition of apoptosis that resulted from miR-770-5p downregulation in A2780S cells. [score:6]
Thus, the anti-oncogenic and cisplatin chemosensitivity-enhancing effects of miR-770-5p in OVC might depend on its ability to downregulate ERCC2 expression (Figure 7). [score:6]
In addition, silencing ERCC2 inhibited DNA damage repair similarly to miR-770-5p upregulation in A2780CP cells (Figure 6). [score:6]
As indicated in Supplementary Figure S1, miR-770-5p expression was upregulated in OV2008 and A2780S cell lines compared to the cisplatin-resistant variants. [score:5]
To confirm the predictive value of miR-770-5p expression for primary chemosensitivity, we used miR-770-5p expression to predict primary chemoresistance in a separate group of patients before treatment with a platinum -based regimen. [score:5]
miR-770-5p expression is reduced in patients with chemotherapy-resistant EOC, and target predictions. [score:5]
To determine how ERCC2 and miR-770-5p act together to modulate cisplatin-resistance, we used siRNAs to silence ERCC2 expression (siERCC2) in A2780S cells transfected with an miR-770-5p inhibitor. [score:5]
Target prediction was performed for miR-770-5p using three computational approaches: Ingenuity Systems (Redwood City CA, USA), MicroCosm Targets version 5, and miRBase. [score:5]
1: A2780S NC, 2: A2780S miR-770-5p inhibitor, 3: A2780S miR-770-5p inhibitor + siERCC2, 4: A2780CP NC, 5: A2780CP miR-770-5p mimics, 6: A2780CP siERCC2. [score:5]
In the CR group, miR-770-5p was strongly expressed in the cancer epithelium, but ERCC2 expression was weak or undetectable in the same tumor tissues from the same patient. [score:5]
Figure 5(A) Flow cytometric detection of apoptosis via Annexin V-FITC/PI staining in cisplatin-sensitive A2780S cells after treatment with cisplatin (20 μM) for 48 h after transfection with miR-770-5p inhibitor, negative control, or miR-770-5p inhibitor + siERCC2. [score:5]
hsa-miR-770-5p was highly expressed in the tumor epithelium (green arrows in ii) of CR patients (i-iv), and ERCC2 expression was absent in the same tumor area (in iv). [score:5]
Unexpectedly, high miR-770-5p expression predicted chemoresistance with an accuracy of up to 81.1% in the retrospective and 76% in prospective assessments, with a 6.128-fold in expression serving as the cutoff value. [score:5]
Overexpression of miR-770-5p inhibits survival of chemo-resistant cell lines after cisplatin treatment. [score:5]
Overexpression of miR-770-5p inhibits survival in cisplatin-chemoresistant cell lines. [score:5]
Two miRNAs (miR-770-5p and hsa-miR-136*, red circle) were more highly expressed (p < 0.0001) in the CR group, and one (hsa-miR-9, green circle) was more highly expressed in the IR group. [score:5]
To determine how ERCC2 modulates chemosensitivity, we used siRNA to silence ERCC2 expression (siERCC2) in A2780S cells transfected with an miR-770-5p inhibitor. [score:5]
Kaplan-Meier survival analysis also indicated that low miR-770-5p expression was associated with shorter overall survival compared to the high expression group (n = 25 for CR and n = 15 for IR, p < 0.001 for CR group, p < 0.05 for IR group). [score:4]
miR-770-5p was downregulated in chemoresistant EOC patients, indicating that miRNAs are involved in the response to platinum -based regimens. [score:4]
To understand the mechanism by which miR-770-5p regulates chemoresistance in OVC, we identified possible target genes using computational approaches. [score:4]
miR-770-5p is downregulated in chemotherapy-resistant EOC patients. [score:4]
Furthermore, silencing ERCC2 expression in A2780S cells treated with the miR-770-5p inhibitor restored chemosensitivity to cisplatin as indicated by both flow cytometry and TUNEL assays (Figure 5). [score:4]
Kaplan-Meier survival analysis revealed that low miR-770-5p expression was associated with shorter overall survival in OVC patients compared to the high miR-770-5p expression group (Figure 2D–2F). [score:4]
Western blotting and semi-quantitative RT-PCR analyses revealed that miR-770-5p negatively regulated ERCC2 expression at both the mRNA and protein levels (Figure 4E). [score:4]
One of these three miRNAs, miR-770-5p, was upregulated 2.9-fold in the CR group versus the IR group (p = 1.66E–06, adjusted p-value = 8.78E–04) (Figure 1A and Supplementary Table S1). [score:4]
To determine whether ERCC2 is a target of miR-770-5p, quantitative and qualitative analysis at both the miRNA and mRNA levels were performed in vivo and in vitro. [score:3]
miR-770-5p expression accurately predicted primary chemotherapy response in this validation cohort (76% accuracy; Figure 2C). [score:3]
In this study, we report that miR-770-5p enhances chemosensitivity at least in part by targeting ERCC2. [score:3]
Figure 4miR-770-5p inhibits ERCC2 in vivo and in vitro(A) Sequence alignment of human miR-770-5p with the 3'-UTR of ERCC2. [score:3]
To confirm this finding, we examined miR-770-5p expression using qRT-PCR and ISH. [score:3]
After transfection with the miR-770-5p inhibitor, A2780S DNA repair abilities increased, suggesting that these cells became more resistant to cisplatin. [score:3]
Taken together, these results indicate that miR-770-5p expression level may serve as a novel predictor and prognostic biomarker of OVC patient response to platinum -based chemotherapy and survival. [score:3]
Based on the above results (Figure 1A–1C), we further confirmed the relationship between miR-770-5p expression and chemosensitivity in the human ovarian cancer cell lines OV2008 and A2780S and their cisplatin-resistant variants C13 and A2780CP, respectively. [score:3]
miR-770-5p inhibits ERCC2 in vivo and in vitro. [score:3]
This finding demonstrates that miR-770-5p expression immediately after primary EOC diagnosis can be used as a biomarker to assist in selecting the appropriate chemotherapy regimen before treatment begins, helping to avoid unnecessary toxicities and enhance quality of life. [score:3]
To confirm the association between miR-770-5p and chemo-resistance in vitro, we transiently transfected OVC cell lines with an miR-770-5p expression vector. [score:3]
As shown in Figure 1B–1C, miR-770-5p expression was lower in IR patients than in CR patients. [score:3]
A Mann-Whitney U test demonstrated that miR-770-5p expression distinguished IR patients from CR patients (p < 0.001). [score:3]
ERCC2 is a potential target of miR-770-5p. [score:3]
Lipofectamine 2000 (Invitrogen) was incubated with pre-miR-770-5p (miRNA mimic), anti-miR-770-5p (inhibitor), or scrambled negative controls (Ambion, mock) at a concentration of 90 nM and incubated in serum-free 1640 for 20 min before being added to cancer cells. [score:3]
We then examined the relationship between miR-770-5p expression and primary chemo-responsiveness in patients in a retrospective study. [score:3]
miR-770-5p expression was higher in CR than in IR samples (p < 0.001). [score:3]
Here, we detected an inverse correlation between miR-770-5p and ERCC2 expression both in tumor specimens from OVC patients who received platinum -based chemotherapy and in vitro. [score:3]
Figure 4C shows the qualitative validation of miR-770-5p and its predicted target, ERCC2, in FFPE serial sections from same EOC patient. [score:3]
To confirm the miRNA-target relationship between miR-770-5p and ERCC2, miRNA and mRNA ISH was performed. [score:3]
A 53-sample training cohort was used to identify the miR-770-5p expression level that predicted clinical outcome. [score:3]
In contrast, IR tumors (v-viii) expressed low levels of hsa-miR-770-5p, but higher levels of ERCC2 (green arrows in viii). [score:3]
Prediction of chemotherapy response and survival rate in EOC patients based on miR-770-5p expression. [score:3]
Quantitative analysis using Image-Pro 6.0 software confirmed an inverse relationship between miR-770-5p and ERCC2 mRNA expression in the CR and IR groups (Figure 4D). [score:3]
The miR-770-5p mimics and inhibitors were designed and chemically synthesized by Ambion (Cat#38422-01; Life Technologies Corporation, Denmark). [score:3]
ERCC2, one of the candidate target genes involved in NER, contains a putative region (nucleotides 279–301 in the human sequence 3'-UTR, NM_000400.2) that matches the seed sequence of hsa-miR-770-5p (Figure 4A). [score:3]
Ectopic miR-770-5p expression increased survival and reduced apoptosis in ovarian cancer cells, suggesting that miR-770-5p also modulates therapeutic response. [score:3]
Figure 3(A) Transfection with pre-miR-770-5p inhibited survival in C13 and A2780CP cells treated with various concentrations of cisplatin compared to mock and negative control groups (n = 10 for all groups). [score:2]
[†], statistically significant difference in miR-770-5p expression compared to either negative control or mock -transfected cells (all p < 0.01). [score:2]
A2780S cells became more resistant to cisplatin after transient transfection -mediated miR-770-5p silencing (Figure 5A–5C). [score:1]
To determine the impact of miR-770-5p on chemoresistance, we performed retrospective and prospective assessments of miR-770-5p as a predictor of primary chemosensitivity before and after patients received a platinum -based regimen. [score:1]
ERCC2 and miR-770-5p modulate sensitivity of ovarian cancer cells to cisplatin -induced apoptosis. [score:1]
The sections were incubated with pre-hybridization buffer (10 mL formamide, 5 mL 20× SSC, 2 mL 50× Denhardt's, 250 μL 20 mg/mL yeast RNA, 1000 μL 10 mg/mL salmon sperm DNA, 0.4 g blocking powder, and 1.75 mL DEPC -treated water) at 55°C for 1 h. Hybridization buffer containing the probes for has-miR-770-5p or ERCC2 was applied to each section and hybridized overnight at 55°C. [score:1]
We then investigated the effects of miR-770-5p overexpression on sensitivity to cisplatin chemotherapy in the resistant cell lines after treatment with various cisplatin concentrations or following various durations of miR-770-5p transfection in vitro. [score:1]
C13 and A2780CP cell survival was also markedly decreased after pre-miR-770-5p transfection and 24 hours of cisplatin treatment (Figure 3D). [score:1]
Overall survival of CR and IR patients divided into high and low miR-770-5p subgroups. [score:1]
The probes used for ISH were hsa-miR-770-5p (Exiqon; Cat#38422-01) and human ERCC2 (an EcoRI-BamH1 fragment with antisense and sense digoxigenin-labeled riboprobes which were in vitro-transcribed from the full-length human ERCC2 coding sequence according to the Boehringer-Mannheim-Roche protocol). [score:1]
Therefore, the miR-770-5p-ERCC2 interaction might be a useful biomarker for predicting chemosensitivity to cisplatin in OVC patients. [score:1]
Effects of ERCC2 on miR-770-5p-modulated chemoresistance in ovarian cancer cells. [score:1]
miR-770-5p levels predict response to platinum -based chemotherapy and survival in OVC patients. [score:1]
Transfection with pre-miR-770-5p reduced C13 and A2780CP cell viability relative to the mock and negative control groups (Figure 3A and 3B). [score:1]
Because the effects of miR-770-5p on DNA repair might explain its ability to modulate cisplatin-resistance in ovarian cancer, we examined the role of ERCC2 in this repair process. [score:1]
These results indicate that the effect of miR-770-5p on cisplatin-sensitivity was at least partly mediated by ERCC2. [score:1]
Preliminary experiments and comprehensive computational analysis identified miR-770-5p as a particularly relevant miRNA. [score:1]
To determine whether ERCC2 is also modulated by miR-770-5p in vitro, the cisplatin-sensitive parental cell lines (OV2008, A2780S) and their resistant variants (C13 and A2780CP) were transfected with anti-miR-770-5p or pre-miR-770-5p, respectively. [score:1]
The same relationship between miR-770-5p and ERCC2 was also observed in IR patients. [score:1]
Schematic mo del depicting mediation of response to cisplatin -based primary chemotherapy by miR-770-5p and ERCC2 OVC patients. [score:1]
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[+] score: 178
Other miRNAs from this paper: hsa-mir-31, hsa-mir-675
Thus, we speculated that downregulation of MEG3 in accordance with the low -expression of miR-770-5p contributed to the upregulation of SRGAP1, resulting in the suppression of neural cell migration, and leading to the development of HSCR. [score:12]
As expected, SRGAP1 siRNA, when co -transfected with MEG3 siRNA or miR-770-5p inhibitor, reversed the suppression of cell migration and proliferation caused by MEG3 siRNA and miR-770-5p inhibitor, suggesting that MEG3 and miR-770-5p acted by upregulating SRGAP1. [score:10]
The results showed that MEG3 was downregulated in HSCR (Figure 1A) and consistent with the expression levels of miR-770-5p (Figure 1B), indicating that low -expression level of miR-770 may have an effect on the development of HSCR. [score:9]
miR-770-5p expression was downregulated, whereas SRGAP1 was upregulated at the mRNA and protein levels (Figure 1E and 1F). [score:9]
To validate SRGAP1 as the target gene of miR-770-5p, two cell lines were transfected with miR-770-5p inhibitor, and SRGAP1 mRNA and protein levels were found upregulated. [score:8]
Results showed that cell migration and proliferation were significantly decreased in cells transfected with the miR-770-5p inhibitor, suggesting that inhibition of miR-770-5p suppresses cell migration and proliferation (Figure 3A). [score:7]
It was found that deprivation of MEG3 expression remarkably reduced miR-770-5p expression (Figure 1E and 1F) in both cells, which indicating that miR-770-5p was regulated by MEG3. [score:6]
miR-770-5P inhibitor suppressed cell migration and proliferation. [score:5]
The lncRNA MEG3, which acts as tumor suppressor, is a precursor of miR-770-5p and plays critical roles in many diseases [18, 19]. [score:5]
Firstly, cells were cultured on 6-well plates and transfected with miR-770-5p inhibitor/mimics, SRGAP1 siRNAs, MEG3 siRNAs, MEG3-overexpression lentivirus and negative control. [score:5]
Moreover, assessment of RNA levels showed that the expression levels of miR-770-5p were consistent with MEG3 expression levels, indicating that MEG3 may function via miR-770-5p. [score:5]
For detection of cell cycle assay, cells, which were transfected with miR-770-5p inhibitor, MEG3 siRNA and infected MEG3-overexpression lentivirus, were harvested and detected by BD Biasciences FACS Calibur Flow Cytometry (BD Biasciences, NJ, USA). [score:4]
Thirdly, cell migration and proliferation assays were used to explore functional changes when the two cell lines were co -transfected with MEG3 siRNA and miR-770 mimics, MEG3-overexpression lentivirus, and miR-770 inhibitor singly. [score:4]
In the present study, MEG3 and miR-770-5p, which is located in its intronic region, were both downregulated in HSCR patients. [score:4]
The lncRNA MEG3 positively correlates with miR-770-5p expression in HSCR patients. [score:3]
SRGAP1 was the target gene for miR-770-5P. [score:3]
To confirm that SRGAP1 is a target gene for miR-770-5p, two independent methods were used. [score:3]
Figure 3 (A) Cell migration and proliferation were significantly decreased in 293T and SH-SY5Y cells transfected with the miR-770-5p inhibitor. [score:3]
However, there were no differences in cell cycle progression or the percentage of apoptotic cells between miR-770-5p inhibitor transfected and control cells (Supplementary Figure 1). [score:3]
SRGAP1 is a downstream target of MEG3/miR-770-5p. [score:3]
These results indicated that miR-770-5p decreased SRGAP1 expression by binding to the 3′-UTR of SRGAP1. [score:3]
ORG, TRAGETSCAN and MIRDB) were used to predict target genes of miR-770-5p. [score:3]
The results showed that SRGAP1 was the target gene of miR-770-5p. [score:3]
To further examine whether SRGAP1 has an effect on cell migration and proliferation, we performed a series of rescue experiments in which 293T and SH-SY5Y cells were co -transfected with miR-770-5p inhibitor and SRGAP1 siRNA, and MEG3 siRNA and SRGAP1 siRNA separately. [score:3]
To determine the role of MEG3 and miR-770-5p in the occurrence of HSCR, we assessed the expression level of MEG3 and miR-770-5p. [score:3]
MEG3, the host gene of miR-770-5p, positively correlates with miR-770-5p expression in HSCR patients. [score:3]
Figure 4 (A, B) SRGAP1 siRNA could partly reverse cell migration and proliferation in 293T and SH-SY5Y cell lines transfected with miR-770-5p inhibitor. [score:3]
The last intron of MEG3 encodes miR-770-5p, which is expressed in senior mammals such as humans, horses, Rhesus monkeys, chimpanzees, the house mouse, and Norway rat. [score:3]
In conclusion, the present study showed that MEG3 plays a role in the pathogenesis of HSCR through miR-770-5p and its downstream target SRGAP1. [score:3]
Figure 1 (A, B, C) The lncRNA MEG3, miR-770-5p and SRGAP1 expression were detected in HSCR patient colon tissues (n=96) and controls (n=96). [score:3]
The mRNA and protein expression of SRGAP1 and miR-770-5p were determined by qRT-PCR and Western blot. [score:3]
Secondly, the SRGAP1 mRNA and protein levels were evaluated by qRT-PCR and western blotting separately after transfected with miR-770-5p inhibitor and control in 293T and SH-SY5Y cells for 48 h. SRGAP1 expression was significantly increased at both mRNA and protein levels in 293T and SH-SY5Y cells (Figure 1E and 1F). [score:3]
In addtion, Cell migration and proliferation changes caused by MEG3 siRNA were partly rescued by miR-770-5p mimics, the same with the change in the overexpression of MEG3 as expected. [score:3]
Given the role of lncRNAs in neural diseases, the importance of the relation between lncRNAs and miRNAs in the pathophysiologic mechanism, and the MEG3 and miR-770-5p were abnormally decreased in HSCR, we speculated that MEG3, miR-770-5p may be involved in the pathogenesis of HSCR. [score:3]
Thus, we investigated the functional involvement of MEG3 and its intron miR-770-5p in HSCR progression and also identified the target gene of the miR-770-5p, SRGAP1, which plays important roles in the development of the nervous system. [score:2]
Cell migration was increased in response to SRGAP1 silencing compared with that in cells transfected with miR-770-5P inhibitor or MEG3 siRNA alone, although it was still lower than that of the control. [score:2]
We firstly confirmed that MEG3 and miR-770-5p play a role in the etiology of HSCR. [score:1]
Co-transfection of miR-770-5p mimics partially rescued the MEG3 siRNA -mediated decreasing in cell migration and proliferation (Figure 4C). [score:1]
These results clearly indicated that the effect of MEG3 on cell migration and proliferation was mediated by the miR-770-5p/SRGAP1 pathway in HSCR. [score:1]
In this study, we explored the mechanism of pathophysiological roles and the potential relationship between lncRNA MEG3 and miR-770-5p, indichating that the lncRNA MEG3/miR-770-5p/SRGAP1 pathway may play important roles in the pathogenesis of HSCR. [score:1]
To determine whether MEG3 functions via the miR-770-5p/SRGAP1 pathway, we firstly transfected 293T and SH-SY5Y cells with MEG3 siRNA. [score:1]
The MEG3/miR-770-5P/SRGAP1 pathway provides a new approach for understanding the etiology of HSCR. [score:1]
Firstly, the wild-type or a mutant seed sequence of SRGAP1 that was shared by miR-770-5p was cloned into the pLG3 vector to yield pLG3-SRGAP1 or pLG3-SRGAP1-mut. [score:1]
To confirm the cellular function of miR-770-5P, we examined the effect of miR-770-5p on cell migration, cell proliferation, cell cycle procession, and apoptosis. [score:1]
The relative luciferase activity of the group co -transfected with PLG3-SRGAP1 and miR-770-5p mimics was significantly decreased (Figure 3B). [score:1]
We speculated that MEG3, miR-770-5p are involved in the pathogenesis of HSCR. [score:1]
Taken together, these results suggested that miR-770-5p is a pivotal mediator in MEG3 -induced HSCR progression. [score:1]
miR-770-5p is located in the intron of the lncRNA MEG3. [score:1]
TOP: The firefly luciferase activity in 293T and SH-SY5Y cells after cotransfection with reporter construct and miR-770-5p mimics. [score:1]
To further elucidate the relationship between MEG3 and miR-770-5p, we transfected the 293T and SH-SY5Y cells with MEG3 siRNA. [score:1]
Nevertheless, the relationship between MEG3, miR-770-5p and the role of MEG3 in HSCR have not been reported. [score:1]
MEG3 effect on cell migration and proliferation was mediated by the miR-770-5p/SRGAP1 pathway in HSCR. [score:1]
We transfected with pRL-SV40, negative control, miR-770-5p mimics, pGL3-SRGAP1 and pGL3-SRGAP1-mut by using Lipofectamine 2000 (Invitrogen Corp, CA, USA). [score:1]
however, the underlying mechanism of miR-770-5p and MEG3 is still unknown. [score:1]
In transfection experiments, synthetic miRNA precursor molecules of miR-770-5p, negative control and siRNA of SRGAP1 and MEG3 (GenePharma, Shanghai, China) were used with Lipofectamine 2000 Reagent (Invitrogen, CA, USA) following the protocol of the manufacturer. [score:1]
Those results suggested that miR-770-5p is a pivotal mediator in MEG3 -induced HSCR progression. [score:1]
Flow cytometric analysis was performed to test the role of miR-770-5p in cell cycle progression and apoptosis. [score:1]
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[+] score: 15
If these genes are bona fide targets, loss of miR-770 that occurs in the associated pUPD syndromes could contribute to the observed phenotypes by increasing the levels of its targeted genes, many of which are implicated in placental, bone, and muscle biology. [score:5]
Meg3/Gtl2: Imprinting, Expression, and miR-770 Figure 4A shows that Meg3/Gtl2 is maternally expressed using an identified Alw26I restriction site polymorphism between CzechII/Ei and 129S1 mice. [score:5]
Meg3/Gtl2: Imprinting, Expression, and miR-770. [score:3]
In addition, Meg3/Gtl2 contains in its last intron (Relative to Accession number Y13832) the evolutionarily conserved microRNA miR-770 (see Figure 2 and Table 2). [score:1]
org/microrna/) Meg3mmu-miR-770 # Bmp1, Bmp15, Capn3, Casq2, Fosb, Lmna, Mb, Obscn, Peg10, Ppp1ca, Sspn, Tmod1, Trp53 Unidentified mmu-miR-673 Camk2a, Camk2b, Camk2d, Camk2g, Dnmt1, Mtpn, Myh6, Ndn, Pax3, Rbl1, Sln, Tnnt1, Wnt1 Unidentifiedmmu-miR-493 # Cacng5, Camk2g, Cdkn1c, Ctcf, Dag1, Fhl1, Fos, Hras1, Jun, Mib2, Mtap, Peg10, Shh, Tmod1 Unidentifiedmmu-miR-337 # Capza2, Des, Dmd, Dnmt3a, Myh8, Mypn, Nfatc1, Plagl2, Pvalb, Sgcb, Snta1, Tpm3, Trp53 Unidentified mmu-miR-540 Akt3, Bmp2, Bmp7, Capzb, Emd, Itga7, Itgb1, Msc, Myog, Nkx2-5, Pten, Rhoa, Sln, Tlx1, Vim Unidentifiedmmu-miR-665 # Casq2, Igf2, Junb, Ldb3, Peg10, Magel2, Nnat, Pax3, Ryr1, Sntb2, Tln1, Tpm2, Trp53, TtnAnti-Peg11 $ mmu-miR-431 # d Camk2b, Casq1, Dtna, E2f1, Fgf4, Gata3, Igf1, Kit, Max, Peg10, Plagl2, Ppp3r1, Sgcd, Tcf21Anti-Peg11 $ mmu-miR-433 # Bmpr1b, Capza1, Creb1, Ctcf, E2f3, Gata6, Isl1, Jak2, Myh9, Peg10, Plagl2, Ppp3r1, Sntg1Anti-Peg11 $ mmu-miR-127 # d e Auts2, Bcl6, Camk2d, Cdc42, Creb5, E2f3, Igf2, Myo1c, Otx1, Plagl2, Pitx2. [score:1]
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[+] score: 15
In detail, we selected two miRNAs with highest (miR-4750-5p) and moderate (miR-328-5p) fold change among the up-regulated miRNAs and two miRNAs with highest (miR-770-5p) and moderate (miR-564) fold change among the down-regulated miRNAs. [score:7]
As for atrial myocardial samples from infants with CHDs, we found significantly different expression of six miRNAs (miR-210-5p with a P-value of 0.014, miR-423-3p with a P-value of 0.034, miR-143-3p with a P-value of 0.018, miR-564 with a P-value of 0.024, miR-770-5p with a P-value of 0.025, and miR-874-5p with a P-value of 0.040) between prior and after CPB (Fig.   4). [score:3]
The blue and orange lines indicate the two main clusters of samples To validate the data obtained from the miRNA microarray, RT-qPCR was performed to re-examine the expression level of nine miRNAs, namely miR-328-5p, miR-4750-5p, miR-210-5p, miR-423-3p, miR-143-3p, miR-564, miR-770-5p, miR-874-5p and miR-93-5p. [score:3]
The significance of the differences in the expression was confirmed for seven miRNAs namely miR-210-5p, miR-423-3p, miR-143-3p, miR-564, miR-770-5p, miR-874-5p and miR-93-5p) (P < 0.05) in the atrial myocardial samples from patients with CHDs after CPB compared to before CPB by RT-qPCR (Fig.   3). [score:2]
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[+] score: 8
f Lentiviral expression of miR-770, miR-136, miR-379, and miR-410 (n = 4) and g RNAi (shRNA) -mediated knockdown of DLK1, MEG3, MEG8, and MEG9 (n = 5) in CD34 [+] HSPCs in vitro. [score:4]
We ectopically expressed four miRNAs representing different clusters and/or miRNA-families: miR-770 located in the intron of MEG3, miR-136 from the miR-127~136 cluster, and miR-379 and miR-410 as the first and last miRNAs from the megacluster (Supplementary Fig.   7a). [score:3]
Among the ncRNAs are several lncRNAs, a box C/D snoRNA cluster, and 54 miRNAs, including the miR-127~136 cluster (7 miRNA-members), the miR-379~410 megacluster (42 miRNAs), and intronic miR-770. [score:1]
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[+] score: 8
Other miRNAs from this paper: hsa-let-7a-1, hsa-let-7a-2, hsa-let-7a-3, hsa-let-7b, hsa-let-7c, hsa-let-7d, hsa-let-7e, hsa-let-7f-1, hsa-let-7f-2, hsa-mir-16-1, hsa-mir-17, hsa-mir-21, hsa-mir-23a, hsa-mir-24-1, hsa-mir-24-2, hsa-mir-25, hsa-mir-26a-1, hsa-mir-26b, hsa-mir-30a, hsa-mir-31, hsa-mir-96, hsa-mir-99a, hsa-mir-16-2, hsa-mir-30c-2, hsa-mir-30d, hsa-mir-182, hsa-mir-183, hsa-mir-211, hsa-mir-217, hsa-mir-218-1, hsa-mir-218-2, hsa-mir-221, hsa-mir-222, hsa-let-7g, hsa-let-7i, hsa-mir-15b, hsa-mir-23b, hsa-mir-30b, hsa-mir-125b-1, hsa-mir-132, hsa-mir-143, hsa-mir-145, hsa-mir-191, hsa-mir-125a, hsa-mir-125b-2, hsa-mir-126, hsa-mir-184, hsa-mir-190a, hsa-mir-195, rno-mir-322-1, rno-let-7d, rno-mir-335, rno-mir-342, rno-mir-135b, hsa-mir-30c-1, hsa-mir-299, hsa-mir-30e, hsa-mir-26a-2, hsa-mir-379, hsa-mir-382, hsa-mir-342, hsa-mir-135b, hsa-mir-335, 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-15b, rno-mir-16, rno-mir-17-1, rno-mir-21, rno-mir-23a, rno-mir-23b, rno-mir-24-1, rno-mir-24-2, rno-mir-25, rno-mir-26a, rno-mir-26b, rno-mir-30c-1, rno-mir-30e, rno-mir-30b, rno-mir-30d, rno-mir-30a, rno-mir-30c-2, rno-mir-31a, rno-mir-96, rno-mir-99a, rno-mir-125a, rno-mir-125b-1, rno-mir-125b-2, rno-mir-126a, rno-mir-132, rno-mir-143, rno-mir-145, rno-mir-183, rno-mir-184, rno-mir-190a-1, rno-mir-191a, rno-mir-195, rno-mir-211, rno-mir-217, rno-mir-218a-2, rno-mir-218a-1, rno-mir-221, rno-mir-222, rno-mir-299a, hsa-mir-384, hsa-mir-20b, hsa-mir-409, hsa-mir-412, hsa-mir-489, hsa-mir-494, rno-mir-489, rno-mir-412, rno-mir-543, rno-mir-542-1, rno-mir-379, rno-mir-494, rno-mir-382, rno-mir-409a, rno-mir-20b, hsa-mir-542, hsa-mir-190b, hsa-mir-543, rno-mir-466c, rno-mir-17-2, rno-mir-182, rno-mir-190b, rno-mir-384, rno-mir-673, rno-mir-674, rno-mir-770, rno-mir-31b, rno-mir-191b, rno-mir-299b, rno-mir-218b, rno-mir-126b, rno-mir-409b, rno-let-7g, rno-mir-190a-2, rno-mir-322-2, rno-mir-542-2, rno-mir-542-3
MiRNAs found to be primarily down-regulated in DHT -treated rats includes rno-miR-770, rno-miR-466c, rno-miR-21, rno-miR-31, rno-miR-182, rno-miR-183, rno-miR-96, rno-miR-132, rno-miR-182, rno-miR-384-3p and rno-miR-184. [score:4]
Thus, it is possible that the down-regulation of miRNAs (rno-miR-770, rno-miR-466c, rno-miR-31, rno-miR-183, rno-miR-96, rno-miR-132, rno-miR-182, rno-miR-384-3p and rno-miR-184) observed in this study could be associated with promoted thecal hyperandrogenesis [37, 38]. [score:4]
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[+] score: 7
They have identified miR-483, miR-877, miR-337-5p, miR-546, and miR-494 as being upregulated, and miR-770-5p, miR-487b, miR-220, miR-212, and miR-712 as downregulated by adenosine signaling in MΦs. [score:7]
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[+] score: 4
The rest of co-expressed clusters were listed for regions at 6q13 (including mir-30a and mir-30c-2), Xp11.23 (including mir-362, mir-500, mir-501, mir-502 and mir-532), 14q32.2 (including mir-134, mir-379 and mir-382), 14q32.31 (including mir-127, mir-432 and mir-770), 9q22.32 (including let-7d, mir-23b and mir-27b) and 7q22.1 (including mir-93 and mir-106b) (Table 3). [score:3]
Loss of regions including 14q32.2 (location of mir-127, mir-432 and mir-770) and 14q32.31 (mir-134, mir-379, and mir-382) were reported in previous studies of renal cancer and osteosarcoma [16], [44]. [score:1]
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[+] score: 3
24 *** hsa-mir-770-5p 19 *** 75.47 *** hsa-mir-93* 9.5 *** 92.1 - Inhibited differentiation & low cell count *** hsa-let-7b* 4.75 *** 28.64 *** hsa-mir-1224-3p 2.38 *** 51.46 *** hsa-mir-1228 2.38 ** 9.43 *** hsa-mir-1249 1.66 *** 53.17 *** hsa-mir-125a-5p 19 *** 69.8 *** hsa-mir-1260 7.12 *** 61.75 *** hsa-mir-1280 11.88 *** 68.95 *** hsa-mir-129-3p 9.5 *** 65.64 - hsa-mir-1296 9.5 *** 36.36 *** hsa-mir-133a/hsa-mir-133b 42.75 * 0.85 *** hsa-mir-150 4.75 *** 60.37 *** hsa-mir-197 4.75 *** 27.79 *** hsa-mir-204 2.85 *** 27.44 *** hsa-mir-328 0.1 ** 30.87 *** hsa-mir-342-3p 33.25 *** 58. [score:3]
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[+] score: 3
It was first described as a paternally imprinted locus encoding a 10-exon RNA [42], and in a notable similarity to the likewise monoallelically expressed H19 (see below), miR-770 derives from the final exon of MEG3 [43]. [score:3]
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[+] score: 3
Besides the conserved start position 771, positions 139 of hsa-miR-1470, 141 of hsa-miR-3622a-3p, 148 of hsa-miR-485-3p, and 582 of hsa-miR-770-5p were highly conserved among more than one thousand sequences of NS1 genes in type 1 while position 137 was predicted start binding position of both hsa-miR-1236 and hsa-miR-1249. [score:1]
The start binding positions 304 of hsa-miR-762 and 308 of hsa-miR-3677 were highly conserved among more than five hundred NS1 genes in type 2 while positions 765 of hsa-miR-637 and 773 of hsa-miR-3663-5p were highly conserved among almost three hundred NS1 sequences in dengue type 3. More than two hundred nucleoprotein (NP) genes of rabies virus were predicted with highly conserved start binding positions 122 of hsa-miR-939, 359 of hsa-miR-770-5p, and 820 of hsa-miR-2277-3p and hsa-miR-638. [score:1]
The start binding positions 304 of hsa-miR-762 and 308 of hsa-miR-3677 were highly conserved among more than five hundred NS1 genes in type 2 while positions 765 of hsa-miR-637 and 773 of hsa-miR-3663-5p were highly conserved among almost three hundred NS1 sequences in dengue type 3. More than two hundred nucleoprotein (NP) genes of rabies virus were predicted with highly conserved start binding positions 122 of hsa-miR-939, 359 of hsa-miR-770-5p, and 820 of hsa-miR-2277-3p and hsa-miR-638. [score:1]
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[+] score: 3
Other miRNAs from this paper: hsa-mir-155, hsa-mir-372, hsa-mir-675
Notably, the last intron of MEG3 encodes the evolutionarily conserved miR-770, a miRNA with a number of putative mRNA targets [159]. [score:3]
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[+] score: 2
Interestingly, 5 of the 42 survival -associated miRs (hsa-miR-770-5p, hsa-miR-541, hsa-miR-485-3p, hsamiR- 656, hsa-miR-668) were encoded in the chromosome 14q32 region. [score:1]
There were 8 common miRs (hsa-miR-429, hsa-miR-221, hsa-miR- 499-5p, hsa-miR-888, hsa-miR-770-5p, hsa-miR-545, hsa-miR-541, hsa-miR-483-3p) between the two sets of survival -associated miRs (Figure S2). [score:1]
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[+] score: 1
PCAT9 stimulates proliferation of osteoarthritic synoviocytes by acting as a sponge for miR-770 [40]. [score:1]
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[+] score: 1
3/3p21.32 −3.91 hsa-miR-487b 14q32.2 −3.82(29) hsa-miR-487a 14q32.2 −3.78 hsa-miR-758 14q32.2 −3.65 hsa-miR-485-5p 14q32.2 −3.60 hsa-miR-138-1* 16q13.3/3p21.32 −3.55 hsa-miR-382 14q32.2 −3.53(12, 29) hsa-miR-504 Xq26.3 −3.45(52) hsa-miR-128 2q21.3/3p22.3 −3.43(12, 14, 51, 59) hsa-miR-490-5p 7q33 −3.42 hsa-miR-770-5p 14q32.2 −3.35 hsa-miR-410 14q32.2 −3.30(29) hsa-miR-432 14q32.2 −3.29 hsa-miR-485-3p 14q32.2 −3.02 hsa-miR-490-3p 7q33 −2.88 hsa-miR-381 14q32.2 −2. [score:1]
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[+] score: 1
931.210.0052-miR-615-3p0.005.45Inf0.0065[9]miR-196b-5p1.0910.179.330.0134[9]miR-127-3p175251.70224611.391.280.0194-miR-208b75.76112.901.490.0217-miR-302a-5p2.676.932.600.0451-miR-2682-5p212.76299.861.410.0451-miR-30a-5p171969.53228298.921.330.0451[8]miR-770-5p333.36445.551. [score:1]
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[+] score: 1
Within the Dlk1–Dio3 cluster, Meg3/Gtl2 contains in its last intron the evolutionarily conserved microRNA miR-770 whereas Meg8 transcripts have the intron-encoded miR-341, miR-1188, and miR-370. [score:1]
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[+] score: 1
MNPT) miR-449a# 3.92 miR-32 3.49 miR-548c-5p 2.71 miR-562 2.56 miR-103-as 2.53 miR-512-3p 2.41 miR-200c* 2.33 miR-147b 2.24 miR-770-5p 2.09 miR-518c* 2.00 miR-517b 1.88 miR-182 1.79 miR-615-3p 1.70 miR-496 1.59 miR-1200 1.58 miR-375 1.54 miR-551a 1.53 *Passanger strand. [score:1]
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