Genome-wide maps of AR binding in prostate cancer cell lines VCaP and VCS2
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE32345 | GEO | 2012/02/01
SECONDARY ACCESSION(S): PRJNA154487
REPOSITORIES: GEO
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Project description: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
2012-02-01 | E-GEOD-32345 | biostudies-arrayexpress
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
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
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).
2015-12-19 | GSE76141 | GEO
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation.We performed ChIP-seq analysis to investigate the role of AR and histone modifications.In addition, by siRNA mediated knockdown of AR-associated factors, changes of AR-binding sites in prostate cancer cells were analyzed.. ChIP-sequence analysis of AR and its associated factors in prostate cancer cells
2015-02-08 | E-GEOD-62492 | biostudies-arrayexpress
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation.We performed ChIP-seq analysis to investigate the role of AR and histone modifications.In addition, by siRNA mediated knockdown of AR-associated factors, changes of AR-binding sites in prostate cancer cells were analyzed..
2015-02-08 | GSE62492 | GEO
Project description:In castration-resistant prostate cancer (CRPC), clinical response to androgen receptor (AR) antagonists is limited mainly due to AR-variants expression and restored AR signaling. The metabolite spermine is most abundant in prostate and it decreases as prostate cancer progresses, but its functions remain poorly understood. Here, we show spermine inhibits full-length androgen receptor (AR-FL) and androgen receptor splice variant 7 (AR-V7) signaling and suppresses CRPC cell proliferation by directly binding and inhibiting protein arginine methyltransferase PRMT1. Spermine reduces H4R3me2a modification at the AR locus and suppresses AR binding as well as H3K27ac modification levels at AR target genes. Spermine supplementation restrains CRPC growth in vivo. PRMT1 inhibition also suppresses AR-FL and AR-V7 signaling and reduces CRPC growth. Collectively, we demonstrate spermine as an anticancer metabolite by inhibiting PRMT1 to transcriptionally inhibit AR-FL and AR-V7 signaling in CRPC, and we indicate spermine and PRMT1 inhibition as powerful strategies overcoming limitations of current AR-based therapies in CRPC.
2023-10-11 | MTBLS8034 | MetaboLights
Project description:Prostate organogenesis is regulated by interactions between mesenchymal and epithelial cells, and via androgen signalling though androgen receptors (AR) expressed in mesenchymal cells. However, there is little knowledge of AR target genes and we have used high resolution genomic methods to examine AR function in subsets of mesenchyme during prostate development. Using ChIP-seq, we defined genomic AR binding sites (ARBS) in microdissected mesenchymal tissues of neonatal male and female rats during prostate growth. By comparing female tissue subsets (ventral mesenchymal pad and urethral smooth muscle) with male tissues (ventral prostate and dorsolateral prostate), we were able to identify sexually dimorphic ARBS. Females had a distinct AR binding profile from males with enrichment of ARBS proximal to gene transcriptional start sites as well as binding to non-classical AR binding sequence motifs. Using both tissue RNA-sequencing and single-cell RNA-sequencing of the same mesenchymal subsets, we identified 128 differentially expressed transcripts between males and females. Comparison of these to ChIP-seq ARBS allowed us to define sexually dimorphic AR target genes. Selected candidates were validated as sexually dimorphic at both the mRNA and protein level in both rat and human developing prostate tissues by qPCR and western blot. Response to testosterone stimulation was examined using ex vivo rat tissue organ cultures and qPCR. In single cell RNAseq data we observed subpopulations of mesenchymal cells in males and females as well as subpopulations common to both. The distribution of AR and target genes did not follow the subpopulation distribution, suggesting that AR action is not restricted by subset identity.Our study is the first to apply multiple transcriptomic approaches to prostate mesenchyme, and we have identified unique AR targets. We have identified sexually dimorphic, androgen responsive mesenchymal target genes that may underlie sexually dimorphic development of the prostate. We suggest that the analysis of transcription factor binding and transcriptomes in cell subsets will be informative when applied to tumour cells and stroma – since these show similar cellular heterogeneity and subset specific activity.
2019-06-30 | GSE116397 | GEO
Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation.We performed ChIP-seq analysis to investigate the role of AR and its associated factors such as coregulators or collaborating factors.In addition, by siRNA mediated knockdown of such factors, changes of AR-binding sites in prostate cancer cells were analyzed. ChIP-sequence analysis of AR and its associated factors in prostate cancer cells
2014-11-14 | E-GEOD-58428 | biostudies-arrayexpress
Project description:Analysis of AR-regulation of gene expression. The hypothesis tested in the present study was that AR influences the expression of genes that participate in important bioprocesses in prostate cancer cells, including cell cycle, DNA replication, recombination and repair. Results provide important information on AR-responsive genes that may be crucial to the cell survival and the progression of prostate cancer. Total RNA obtained from AR siRNA-transfected prostate cancer cells compared to negative control siRNA-transfected prostate cancer cells 48 h after siRNa transfection.
2013-07-28 | E-GEOD-49285 | biostudies-arrayexpress