Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA264150 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To identify the direct target of miR-490-3p, we used whole genome microarray expression profiling to screen for genes potentially regulated by the microRNA. AGS cells were transfected with control mimics or miR-490-3p mimics and gene expression was determined 72 hours after transfection.
2014-10-18 | E-GEOD-62453 | biostudies-arrayexpress
Project description:To identify the direct target of miR-490-3p, we used whole genome microarray expression profiling to screen for genes potentially regulated by the microRNA.
2014-10-18 | GSE62453 | GEO
Project description:Oxaliplatin (oxPt) resistance in colorectal cancers (CRC) is a major unsolved problem. Consequently, predictive markers and a better understanding of resistance mechanisms are urgently needed. To investigate if the recently identified predictive miR-625-3p is functionally involved in oxPt resistance, stable and inducible models of miR-625-3p dysregulation were analyzed. Ectopic expression of miR-625-3p in CRC cells led to increased resistance towards oxPt. The mitogen-activated protein kinase (MAPK) kinase 6 (MAP2K6/MKK6) – an activator of p38 MAPK - was identified as a functional target of miR-625-3p, and, in agreement, was down-regulated in patients not responding to oxPt therapy. The miR-625-3p resistance phenotype could be reversed by anti-miR-625-3p treatment and by ectopic expression of a miR-625-3p insensitive MAP2K6 variant. Transcriptome, proteome and phosphoproteome profiles revealed inactivation of MAP2K6-p38 signaling as a possible driving force behind oxPt resistance. We conclude that miR-625-3p induces oxPt resistance by abrogating MAP2K6-p38 regulated apoptosis and cell cycle control networks.
2017-03-29 | MSV000080762 | MassIVE
Project description:Genes regulated by miR-127-3p in glioblastoma cell line
| PRJNA216956 | ENA
Project description:Background: Circulating microRNAs (miRNAs) have been suggested as candidate biomarkers of frailty, a complex multidomain geriatric syndrome associated with a higher risk of poor outcomes. However, few studies have adopted an unbiased approach to screen for plasma miRNAs associated with frailty independently of common risk factors and little is known relatively to their putative etiopathogenic role. Methods: Leveraging a cohort recruited for a randomized trial testing the effect a remote rehabilitation intervention on frailty in elderlies with cardiovascular diseases (CVD), we tested plasma samples from 24 people, 12 frail and 12 not frail according to the EFT scale and matched for all the other clinical characteristics, to search for miRNAs associated with frailty through small RNA-Sequencing. From this analysis, we selected the 11 most significantly deregulated miRNAs and quantified them in the entire cohort (n=197) through quantitative RT-PCR. Then, we explored the candidate pathways targeted by miRNAs significantly deregulated in frailty through bioinformatics analyses and tested the effect of miR-181b-3p and miR-490-5p overexpression on cellular senescence and inflammation in endothelial cells. Results: We found that plasma levels of miR-181b-3p, miR-490-5p, and miR-500a-5p were increased, while miR-511-5p was reduced, in people with frailty compared with non-frail individuals, also after adjustment for age. Bioinformatics analysis of the frailty-upregulated miRNAs suggested cell cycle and cellular response to DNA damage, two recognized drivers of aging, as regulated biological processes for both miR-181b-3p and miR-490-5p. Overexpression of these two miRNAs through transient transfection in endothelial cells promoted a prototypical cellular senescence response accompanied by a pro-inflammatory phenotype, as assessed through SA-Beta Gal staining and increased expression of multiple senescence and inflammatory markers at both mRNA and protein levels. Conclusions: Overall, these data suggest that circulating levels of miR-181b-3p, miR-490-5p, miR-500a-5p and miR-511-5p might serve as markers of frailty in old people with CVD and that miR-181b-3p and miR-490-5p might be functionally linked to the etiopathogenesis of the syndrome through their effects on cellular senescence and inflammation.
2026-06-10 | GSE331433 | GEO
Project description:Applying Next Generation Sequencing technique we compared the miRNA expression pattern of tumor tissue sample of 6 GPs and peritumoral region of 6 lower grade (I-II) Glioma patients, serving as control group. To determine the difference on miRNA expresion level between GBM and control cases, we performed cluster analysis on the NGS dataset of 6 replicates for each of the two goups of samples with iDEP 96 software. In order to characterize the extent of up- or downregulation, log2FC values were calculated using the iDEP.96 web tool applying the DESeq2 algorithm. On the base of that 117 known miRNAs were identified to be differentially expressed using a threshold of false discovery rate (FDR) <0.05 and fold-change> 2 during the analysis. Among them, 35 miRNAs were upregulated (log2FC > 2) and 82 miRNAs were downregulated (log2FC < -2) with biological revelance in tissue samples comparing with the control samples. To validate our results obtained by NGS, five upregulated miRNAs: hsa-miR-196a-5p, hsa-miR-21-3p, hsa-miR-92b-5p, hsa-miR-10b-3p, hsa-miR-503-5p and three downregulated miRNAs: hsa-mir-383-5p, hsa-mir-490-3p, hsa-mir-1224-3p were chosen for RT-qPCR analysis. As the result of that hsa-miR-196a-5p, hsa-miR-21-3p, and hsa-miR-10b-3p was significantly upregulated while hsa-mir-383-5p and hsa-mir-490-3p was significantly downregulated, compared with those in the control samples. The other three miRNAs: hsa-miR-1224-3p, hsa-miR-92b-5p, hsa-miR-503-5p did not show significant difference between the control group and GPs.
2024-10-31 | GSE244332 | GEO