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FoxA1 specifies unique androgen and glucocorticoid receptor binding events in prostate cancer cells (HTS)

ABSTRACT: We report the androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell lines, LNCaP-1F5 and VCaP in response to physiological androgen 5a-dihydrotestosterone (DHT) using ChIP-sequencing. We compare the AR recruitment by DHT to that by partial agonist/antagonist cyproterone acetate (CPA), mifepristone (RU486) and bicalutamide (Bica) in LNCaP-1F5 cells. We also report the role of glucocorticoid receptor recruitment in presence of dexamethasone (Dex) in androgen responsive prostate cancer cells. The AR and GR cistrome analysis is subsequently compared with gene expression data and RNA Pol II analysis. The ChIP-seq has been performed using AR, GR, RNA Pol II antibodies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE39879 | GEO | 2013/02/05

SECONDARY ACCESSION(S): PRJNA171947

REPOSITORIES: GEO

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FoxA1 specifies unique androgen and glucocorticoid receptor binding events in prostate cancer cells (HTS)

Project description:We report the androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell lines, LNCaP-1F5 and VCaP in response to physiological androgen 5a-dihydrotestosterone (DHT) using ChIP-sequencing. We compare the AR recruitment by DHT to that by partial agonist/antagonist cyproterone acetate (CPA), mifepristone (RU486) and bicalutamide (Bica) in LNCaP-1F5 cells. We also report the role of glucocorticoid receptor recruitment in presence of dexamethasone (Dex) in androgen responsive prostate cancer cells. The AR and GR cistrome analysis is subsequently compared with gene expression data and RNA Pol II analysis. The ChIP-seq has been performed using AR, GR, RNA Pol II antibodies. Examination of AR and GR binding sites in LNCaP-1F5 and VCaP cells in presence of DHT and Dex respectively. Further analysis of AR binding sites in LNCaP-1F5 cells treated with partial agonist/antagonists, CPA, RU486 and Bica. Additionally RNA Pol II mapping is performed in cells treated with DHT and Dex.

2013-02-05 | E-GEOD-39879 | biostudies-arrayexpress

FoxA1 specifies unique androgen and glucocorticoid receptor binding events in prostate cancer cells (mRNA)

Project description:We report the androgen receptor recruitment to the chromatin of androgen responsive prostate cancer cell lines, LNCaP-1F5 and VCaP in response to physiological androgen 5a-dihydrotestosterone (DHT) using ChIP-sequencing. We compare the AR recruitment by DHT to that by partial agonist/antagonist cyproterone acetate and mifepristone (RU486) in LNCaP-1F5 cells. We also report the role of glucocorticoid receptor recruitment in presence of dexamethasone (Dex) in androgen responsive prostate cancer cells. The AR and GR cistrome analysis is subsequently compared with gene expression data and RNA Pol II analysis. The ChIP-seq has been performed using AR, GR, RNA Pol II antibodies. Expression profiling by microarray of LNCaP-1F5 cells treated with vehicle, 100 nM 5a-dihydrotestosterone (DHT), 100 nM dexamethasone (Dex), 1000 nM cyproterone acetate (CPA), 100 nM mifepristone (RU486) and combination of 100 nM DHT,100 nM Dex for 24 hours.

2013-02-05 | E-GEOD-39654 | biostudies-arrayexpress

FoxA1 specifies unique androgen and glucocorticoid receptor binding events in prostate cancer cells (mRNA)

2013-02-05 | GSE39654 | GEO

Dual Role of FoxA1 in Androgen Receptor Binding to Chromatin, Androgen Signaling and Prostate Cancer [ChIP_seq, DHS_seq]

2011-09-14 | E-GEOD-30623 | biostudies-arrayexpress

Dual Role of FoxA1 in Androgen Receptor Binding to Chromatin, Androgen Signaling and Prostate Cancer [Expression Array]

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.

2011-09-13 | E-GEOD-30622 | biostudies-arrayexpress

Dual Role of FoxA1 in Androgen Receptor Binding to Chromatin, Androgen Signaling and Prostate Cancer [Expression Array]

2011-09-14 | GSE30622 | GEO

Dual Role of FoxA1 in Androgen Receptor Binding to Chromatin, Androgen Signaling and Prostate Cancer [ChIP_seq, DHS_seq]

2011-09-14 | GSE30623 | GEO

Ligand-Dependent Enhancer Activation Regulated by Topoisomerase-I Activity

Project description:The discovery that enhancers are regulated transcription units, encoding eRNAs, has raised new questions about the mechanisms of their activation. Here, we report an unexpected molecular mechanism that underlies ligand-dependent enhancer activation, based on DNA nicking to relieve torsional stress from eRNA synthesis. Using dihydrotestosterone (DHT)-induced binding of androgen receptor (AR) to prostate cancer cell enhancers as a model, we show rapid recruitment, within minutes, of DNA topoisomerase I (TOP1) to a large cohort of AR-regulated enhancers. Furthermore, we show that the DNA nicking activity of TOP1 is a prerequisite for robust eRNA synthesis and enhancer activation and is kinetically accompanied by the recruitment of ATR and the MRN complex, followed by additional components of DNA damage repair machinery to the AR-regulated enhancers. Together, our studies reveal a linkage between eRNA synthesis and ligand-dependent TOP1-mediated nicking - a strategy exerting quantitative effects on eRNA expression in regulating AR-bound enhancer-dependent transcriptional programs. Genome-wide binding analysis of AR, TOP1, MRE11 in prostate cancer cell line LNCaP with or without 5alpha-dihydrotestosterone (DHT) treatment. Nascent RNA analysis by global nuclear run-on (GRO-seq) in LNCaP cells transfected with siRNA with or without DHT treatment. Distribution of transcriptionally engaged RNA Pol II in LNCaP cells with or without DHT treatment by precision nuclear run-on and sequencing (PRO-seq).

2015-01-22 | E-GEOD-63202 | biostudies-arrayexpress

Genome-wide mapping of retinoblastoma (Rb) binding sites in prostate cancer cell lines VCaP and LNCaP

Project description:Although well characterized as a transcriptional activator, androgen receptor (AR) can also function as a direct transcriptional repressor in prostate cancer cells. The major targets of the AR repressive function are genes mediating DNA synthesis. In this study, we found that AR was recruited to the majority of these DNA synthesis genes and rapidly repressed their transcription. This direct AR mediated repression was enhanced in prostate cancer cells expressing higher levels of AR, and was mediated by recruitment of hypophosphorylated retinoblastoma protein (Rb). Examination of Rb binding in 4 hours DHT treated prostate cancer cell lines VCaP and LNCaP

2015-12-19 | E-GEOD-76141 | biostudies-arrayexpress

Glucocorticoid Receptor and Androgen Receptor DNA binding in LREX'

Project description:LREX' are a LnCAP/AR subline with natural expresison of the glucocorticoid receptor. We used the model to compare the AR and GR cistromes in prostate tissue. We determined the GR cistrone in the presence of Dex (100nM) treatment and the AR cistrome in the presene of DHT (1nM) treatment.

2013-12-27 | E-GEOD-51497 | biostudies-arrayexpress

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