Unknown,Transcriptomics,Genomics,Proteomics

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MicroRNA profiling in Pten knockout mouse thymus cells

ABSTRACT: MicroRNA profiling in Pten knockout mouse thymus cells. microRNAs (miRs) are short noncoding RNAs of 20â22 nucleotides that function to regulate gene expression at the posttranscriptional level. They play fundamental roles in the regulation of cellular proliferation, differentiation, and apoptosis. miRs are dysregulated in many types of cancer, including T-ALL (T cell lymphoblastic leukemia). miRs can function as oncogenes, favoring the initiation and progression of cancers, or as tumor suppressors, preventing tumorigenesis. The biological functions of miRs in T-ALL are largely unknown. In human T-ALL patients, recurrent mutations in the Phosphatase and tensin homolog (PTEN) gene are common, consistent with Pten-knockout mice developing T-ALL. To better understand T-ALL pathogenesis and identify new therapeutic targets in T-ALL, we developed a Pten-knockout T-ALL mouse model and the mice developed T-ALL within 3 months as expected. We profiled the miRs in the Pten-deficient mouse T-ALL. A576, A577, A578 and A579 are PTEN-knockout mouse T-ALL samples. A580 andA 581 are wild-type mouse thymocytes.

ORGANISM(S): Mus musculus

SUBMITTER: Tian Yuan

PROVIDER: E-MTAB-5053 | 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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MicroRNA profiling in Pten knockout mouse thymus cells

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