Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of murine neurosphere cultures carrying a Bcl2 transgene and treated with histone deacetylase inhibitor Trichostatin A and demethylating agent AzaC to study DNA methylation and histone deacetylation in neural stem cells.

ABSTRACT: Neurosphere cultures were established from individually isolated E 14.5 forebrains of mouse embryos that carry a bcl2 transgene. Single-cell suspensions were prepared, seeded at 1x105 cells/ml and treated for two days with 150 nM Trichostatin A (TSA; histone deacetylase inhibitor), 500 nM 5-Aza-2-deoxycytidine (AzaC; demethylating agent) or both compounds, or left untreated. Two independent experiments were performed.

ORGANISM(S): Mus musculus

SUBMITTER: Martin Zenke

PROVIDER: E-GEOD-587 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Pluripotency associated genes are reactivated by chromatin-modifying agents in neurosphere cells.

Ruau David D Ensenat-Waser Roberto R Dinger Timo C TC Vallabhapurapu Duttu S DS Rolletschek Alexandra A Hacker Christine C Hieronymus Thomas T Wobus Anna M AM Müller Albrecht M AM Zenke Martin M

Stem cells (Dayton, Ohio) 20080117 4

Chromatin architecture in stem cells determines the pattern of gene expression and thereby cell identity and fate. The chromatin-modifying agents trichostatin A (TSA) and 5-Aza-2'-deoxycytidine (AzaC) affect histone acetylation and DNA methylation, respectively, and thereby influence chromatin structure and gene expression. In our previous work, we demonstrated that TSA/AzaC treatment of neurosphere cells induces hematopoietic activity in vivo that is long-term, multilineage, and transplantable. ...[more]

PMID: 18203677

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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.

Dataset Information

Transcription profiling of murine neurosphere cultures carrying a Bcl2 transgene and treated with histone deacetylase inhibitor Trichostatin A and demethylating agent AzaC to study DNA methylation and histone deacetylation in neural stem cells.

Publications

Pluripotency associated genes are reactivated by chromatin-modifying agents in neurosphere cells.

Similar Datasets

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