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Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program

ABSTRACT: Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program

PROVIDER: PRJNA238234 | ENA |

REPOSITORIES: ENA

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Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program [array]

Project description:Previous studies have shown that FOXA1 defines prostatic AR binding events, the underlying mechanisms of which, however, are incompletely understood. To test whether ectopic AR and FOXA1 can activate AR target genes, we performed adenoviral of LacZ, AR, FOXA1 or AR+FOXA1 proteins in DU145 cells, followed by microarray analysis of these cells.

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Project description: Not available

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Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-06-02 | E-GEOD-55007 | biostudies-arrayexpress

Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:Cooperativity and Equilibrium with FOXA1 Define Androgen Receptor Transcriptional Program [array]

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Project description:This SuperSeries is composed of the following subset Series: GSE30622: Dual Role of FoxA1 in Androgen Receptor Binding to Chromatin, Androgen Signaling and Prostate Cancer [Expression Array] GSE30623: Dual Role of FoxA1 in Androgen Receptor Binding to Chromatin, Androgen Signaling and Prostate Cancer [ChIP_seq, DHS_seq] Refer to individual Series

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Project description:We report the dual role of FoxA1 in androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell line LNCaP-1F5 using ChIP-sequencing. Depletion of FoxA1 reprograms both androgen and glucocorticoid receptor recruitment and subsequent gene expression. The ChIP-seq has been performed using AR, FoxA1, GR, H3K4me2 antibodies. We have also mapped the DNaseI-hypersensitive sites (DHS) using deep sequencing. LNCaP-1F5 cells were depleted of FoxA1 using siRNAs. Parental cells and FoxA1 depleted cells (siFoxA1) were treated with vehicle or 100 nM DHT or (100 nM DEX) for 24 hours followed by RNA isolation and hybridization to Illumina arrays. All the experiments have been performed in biological duplicates. Parental cells treated with DHT (or DEX) were analyzed for differentially expressed genes compared to vehicle treated parental cells. Similarly siFoxA1 cells treated with DHT (or DEX) were analyzed for differentially expressed genes compared to vehicle treated siFoxA1 cells.

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