Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Expression data from transfection of U87 glioma cells with miR-376a* for 72 hours

ABSTRACT: Several biological pathways can be under the regulation of miRNAs. These pathways can be indentified by the enforced expression of a miRNA and analysing the expression data for enrichment of specific pathways represented among the genes differentially expressed upon miRNA overexpression. We transfected unedited miR-376a* (376a*A) and edited miR-376a* (376a*G) into U87 cells to identify differentially regulated transcripts. List of differentially expressed genes were subject to pathway enrichment analysis to identify specific biological processes regulated by each of miR-376a*A and miR-376a*G. U87 cells (100,000) were transfected with 50 nM of miR-376a*A, miR-376a*G or miR-control. Following incubation for 72 hours, total RNA was isolated from transfected cells. For each (miR-376a*A or miR-376a*G), genes differentially expressed upon miRNA transfection were determined based on comparison with miR-control-transfected samples. Biological triplicates were used for each sample type.

ORGANISM(S): Homo sapiens

SUBMITTER: Yukti Choudhury

PROVIDER: E-GEOD-34456 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:MicroRNAs (miRs) are small non-coding RNAs that can function as tumor suppressor genes. We previously reported that miR-1 is among the most consistently down-regulated miRs in primary human prostate tumors. In this follow-up study, we further corroborated this finding in an independent dataset and made the novel observation that miR-1 expression is further reduced in distant metastasis and is a predictor of disease recurrence. Moreover, we performed in vitro experiments to explore the candidate tumor suppressor function of miR-1. Cell-based assays showed that miR-1 is epigenetically silenced in human prostate cancer cells. Overexpression of miR-1 in these cells led to growth inhibition and down-regulation of genes in pathways regulating cell cycle progression, mitosis, DNA replication/repair, and actin dynamics. This observation was further corroborated with protein expression analysis and 3’-UTR-based reporter assays, indicating that genes in these pathways are either direct or indirect targets of miR-1. A gene set enrichment analysis revealed that miR-1-mediated tumor suppressor effects are globally similar to those of histone deacetylase inhibitors. Lastly, we obtained preliminary evidence that miR-1 alters gH2A.X marker expression and affects the cellular organization of F-actin and filipodia formation. In conclusion, our findings indicate that miR-1 acts as a tumor suppressor in prostate cancer by influencing multiple cancer-related processes and by inhibiting cell proliferation and motility. In this study we monitored global miRNA expression changes in prostate cancer LNCaP cells treated with the epigenetic compounds 5-Azacytidine (5-AzaC) and/or trichostatin A (TSA). Cells were treated with epigenetic drugs for 36 hours and total RNA was isolated for hybridization to miRNA microarrays. 5 independent experiments were performed (n=4 for combined treatment). The candidate prostate tumor suppressor miRNAs, miR-1, miR-206, and miR-27 were up-regulated in LNCaP cells for Affymetrix microarray analysis. LNCaP cells were transfected with pre-miR oligos and 24 hr post-transfection total RNA was collected for microarray analysis; total of three independent experiments.

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Expression data from transfection of U87 glioma cells with miR-376a* for 72 hours

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