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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide maps of AR binding in prostate cancer cell lines VCaP and VCS2

ABSTRACT: We report the high-throughput profiling of AR binding in prostate cancer cells. Examination of AR binding in prostate cancer cell lines VCaP and VCS2

ORGANISM(S): Homo sapiens

SUBMITTER: Housheng He

PROVIDER: E-GEOD-32345 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Androgen receptor gene expression in prostate cancer is directly suppressed by the androgen receptor through recruitment of lysine-specific demethylase 1.

Cai Changmeng C He Housheng Hansen HH Chen Sen S Coleman Ilsa I Wang Hongyun H Fang Zi Z Chen Shaoyong S Nelson Peter S PS Liu X Shirley XS Brown Myles M Balk Steven P SP

Cancer cell 20111001 4

Androgen receptor (AR) is reactivated in castration-resistant prostate cancer (CRPC) through mechanisms including marked increases in AR gene expression. We identify an enhancer in the AR second intron contributing to increased AR expression at low androgen levels in CRPC. Moreover, at increased androgen levels, the AR binds this site and represses AR gene expression through recruitment of lysine-specific demethylase 1 (LSD1) and H3K4me1,2 demethylation. AR similarly represses expression of mult ...[more]

PMID: 22014572

Similar Datasets

AR binding in prostate cancer cell lines VCaP and VCS2

Project description:This SuperSeries is composed of the following subset Series: GSE32344: Expression profilling of prostate cancer VCaP and VCS2 cells GSE32345: Genome-wide maps of AR binding in prostate cancer cell lines VCaP and VCS2 Refer to individual Series

2012-02-01 | E-GEOD-32356 | biostudies-arrayexpress

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

Regulation of androgen receptor signaling by Oct1 recruitment in prostate cancer

Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed ChIP sequence analysis in AR-positive prostate cancer cell lines, LNCaP and VCaP. In addition, we also examined the effect of PI polyamide specificly inhibit Oct1 binding to AR occupied-regions. ChIP sequence analysis of AR binding sites and epigenetic condition in two prostate cancer cells

2016-04-01 | E-GEOD-77770 | biostudies-arrayexpress

Tissue-specific pioneer factors associate with androgen receptor cistromes and transcription programs. [ChIP-Seq]

Project description:We report the in vivo androgen receptor (AR) binding sites in murine prostate, epididymis and kidney in response to physiological androgen testosterone using ChIP-sequencing and gene expression profiling by microarray. From AR cistrome analysis, we identified tissue-specific collaborating factors i.e. FoxA1 in prostate, Hnf4a in kidney and AP2a in epididymis and validated by ChIP-seq. The ChIP experiments have been performed using antibodies specific to AR, FoxA1, Hnf4a, AP-2a and IgG non-specific antibody as a negative control. Examination of AR binding sites in murine androgen-responsive tissues prostate, epididymis and kidney using ChIP-seq. Further analysis of AR cistromes led to identification of tissue-specific collaborating factors and these collaborating factors are validated by ChIP-seq from the same tissues. Two parallel IgG samples were sequenced, merged together and used as a control data set. Parallel ChIP-seq samples were sequenced and merged for each replicate wherever required to contain approximately the same amount of reads across all tissues and conditions. All ChIP-seq experiments are performed in biological duplicates except for the castrated conditions.

2014-01-21 | E-GEOD-47192 | biostudies-arrayexpress

Hes6 drives a critical AR transcriptional program to induce castration resistant prostate cancer through activation of an E2F1-mediated cell cycle network

Project description:Castrate-resistant prostate cancer (CRPC) is poorly characterized and heterogeneous and while the androgen receptor (AR) is of singular importance, other factors such as c-Myc and the E2F family also play a role in later stage disease. Here we show that Hes6 is up-regulated in aggressive human prostate cancer and drives castration-resistant tumour growth in the absence of ligand binding by enhancing the transcriptional activity of the AR, which is preferentially directed to a regulatory network enriched for other transcription factors including E2F1. In the clinical setting, we have uncovered a Hes6-associated signature that predicts poor outcome in prostate cancer, which can be pharmacologically targeted with restoration of sensitivity to castration. AR and E2F1 ChIPseq from multiple simultaneous LNCaP cell replicates with and without bicalutamide

2014-04-17 | E-GEOD-49832 | biostudies-arrayexpress

The ETS family member GABPa mediates the development of castrate-resistant prostate cancer (ChIP-Seq)

Project description:In prostate cancer, the androgen receptor (AR) is a key transcription factor at all disease stages. We recently showed that during progression to castrate-resistant prostate cancer the AR acquires the ability to bind to a distinct set of genomic sites in tissue samples and that some of the genes that are regulated by the AR in these conditions correlate with poor prognosis. Based on this work we hypothesised that the AR is reprogrammed through interactions with other transcription factors. In the present study we show that GABPÃ¡, an ETS transcription factor which is upregulated in CRPC, is an AR-interacting transcription factor. Ectopic expression of GABPA in prostate cancer cell-lines enables them to acquire some of the molecular and cellular characteristics of CRPC tissues as well as more aggressive growth phenotypes. VCaP prostate cancer cells and Jurkat lymphoma cells were studied for the ETS factors ERG and GABPa binding sites. Each sample was compared to its input.

2014-05-21 | E-GEOD-49091 | biostudies-arrayexpress

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

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. Examination of AR, FoxA1, GR, H3K4me2 binding sites and DHS sites in parental and FoxA1 depleted LNCaP-1F5 cells.

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

Genomic mapping of ERG, AR, histone H3 monomethyl-K4, histone H3 trimethyl-K4 binding sites in mouse prostates in WT, ERG overexpression, Pten loss mouse prostates

Project description:Translocation of ETS transcription factors including ERG and ETV1 occur in half of all prostate cancers. We generated a mouse model of ERG ovexpression (Rosa26-ERG) which when crossed into prostate specific probasin-Cre, expressed ERG specifically in the prostate. We crossed Rosa26-ERG into Pten flox/flox allele to generate compound GEMM mouse. Here, we determined the genomic binding sites of ERG, AR, and the histone marks H3K4me1 and H3K4me3 that maps enhancers and promoters respectively in the prostates of these mice. The prostate of four six month old mice of each genotype were pooled. The chromatin was isolated and ChIP-Seq performed.

2013-06-13 | E-GEOD-47119 | biostudies-arrayexpress

The cistrome and transcriptome landscape of androgen receptor splice variants in castration-resistant prostate cancer cells

Project description:The spliced variant forms of androgen receptor (AR-Vs) have been identified recently in castration-resistant prostate cancer (CRPC) cell lines and clinical samples. Here we identified the cistrome and transcriptome landscape of AR-Vs in CRPC cell lines and determine the clinical significance of AR variants regulated gene.The AR variants binding sites can be identified in 22Rv1 cell line in the absence of androgen. Knocking down full-length AR (AR-FL) doesn't affect AR-Vs binding sites in genome-wide. A set of genes were identified to be regulated uniquely by AR-Vs, but not by AR-FL in androgen-depleted condition. Integrated analysis showed that some genes may be modulated by AR-Vs directly. Unsupervised clustering analysis demonstrated that AR variants gene signature can separate not only the benign and malignant prostate tissue, but also the localized prostate cancer and metastatic CRPC specimens. Some genes modulated uniquely by AR variants were also identified to correlate with the Gleason Pattern of prostate cancer and PSA failure. We conclude that AR spliced variants bind to DNA independent of full-length AR, and can modulate a unique set of genes which is not regulated by full-length AR in the absence of androgen. AR variants gene signature correlate with CRPC and prostate cnacer disease progress. Androgen receptor (AR) binding sites in human prostate cancer 22Rv1 cell lines were studied using ChIP-seq. ChIP enriched and input DNA were sequenced using Illumina HiSeq 2000.

2014-09-10 | E-GEOD-58478 | biostudies-arrayexpress

Effect of ETV1 knockdown on genome wide AR binding in LNCaP Cells

Project description:Translocation of ETS transcription factors including ERG and ETV1 occur in half of all prostate cancers. LNCaP cells harbor an ETV1 translocation. We performed ChIP-Seq analysis to determine the role of ETV1 on AR binding. The localization of enhancers were determined by H3K4me1 ChIP-Seq. To determine ETV1 and H3K4me1 localization, logarithmically growing cells

2013-06-13 | E-GEOD-47120 | biostudies-arrayexpress

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