AR binding in prostate cancer cell lines VCaP and VCS2
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Housheng He
PROVIDER: E-GEOD-32356 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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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:Microarray experiments were performed for VCaP and VCS2 cells with and without androgen stimulation The RNA samples were extracted from VCaP and VCS2 cells treated with Ethanol or 10nM DHT for 24 hours. RNA was submitted to Dana-Farber Cancer Institute Microarray Core Facility for hybridyzation.
2012-02-01 | E-GEOD-32344 | 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:Prostate cancer is the most common cancer in men and androgen receptor (AR) downstream signalings promote prostate cancer cell proliferation. To investigate the AR signaling, we performed directional RNA sequence analysis in AR positive prostate cancer cell line, LNCaP and VCaP. Using Noncode and GENCODE data sets. We identified androgen-regulated long non-coding RNAs (lncRNAs) in prostate cancer cells. Directional RNA sequence analysis of androgen-regulated lncRNAs in prostate cancer cells
2016-08-01 | E-GEOD-82223 | biostudies-arrayexpress
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
Project description:Vitamin D induces anti-proliferative and differentiating effects in prostate cancer. Thus calcitriol, the hormonally active form of Vitamin D, and its analogs have been extensively studied in prostate cancer cells. Yet despite its importance, relatively little is known about the genome-scale mechanisms by which Vitamin D, through its cognate nuclear vitamin D receptor (VDR), exerts its regulatory functions at the genomic level. In this study, we defined VDR transcriptional networks in the LNCaP prostate cancer cell line by mapping the genomic binding sites of VDR and by identifying differentially expressed genes upon calcitriol treatment. We found that VDR and androgen receptor (AR) antagonistically regulate a subset of cell cycle-related genes that are over-expressed in prostate cancer tumors. The expression balance of these genes is partially regulated through the competition dynamics between AR and VDR binding to shared cis-regulatory elements. On such shared elements, we found that FOXA1 mediates this competition by serving as a pioneering factor for both AR and VDR binding. We also found significant enrichment of AR-, VDR-, and AR/VDR overlapping binding sites in prostate cancer-associated single-nucleotide polymorphism (SNP) intervals identified from genome-wide association studies (GWAS), providing genetic evidence to link AR, VDR and their crosstalk to prostate cancer susceptibilities. In particular, we found that in a cis-regulatory element of the RFX6 gene implicated in prostate cancer progression, an allelic variant increases prostate cancer risk by switching the antagonism between AR and VDR into a synergistic interaction. Examination of AR, VDR, and FOXA1 binding in LNCaP cells, in biological replicates
2015-08-01 | E-GEOD-64656 | biostudies-arrayexpress
Project description:Deregulation of the Androgen Receptor (AR) transcriptional network is a common hallmark in prostate cancers. To achieve its precise transcriptional role, AR needs to co-operate specifically with a plethora of cofactors. In prostate cancers, AR transcription collaborators are frequently aberrantly over-expressed, altering the AR signaling pathway to one that promotes oncogenesis. Recently, the prostate cancer recurrent fusion gene, ERG, was shown to promote tumor progression by acting as a repressor of AR signaling. However, the exact mechanics and the functional consequences associated with this crosstalk between ERG and AR still remains relatively unknown. Interestingly, through chromatin immunoprecipitation coupled with massively parallel sequencing, we discover that ERG and other commonly over-expressed transcriptional co-repressors (HDAC1, HDAC2, HDAC3 and EZH2) are wired into an AR centric transcriptional network via a spectrum of distal enhancers and/or proximal promoters. We show that ERG represses several AR target genes involved in epithelial differentiation. Furthermore, we demonstrated that suppression of the androgen induced gene, Vinculin, by ERG and histone deacetylases increases cancer cell invasiveness. From our results, we propose that ERG, histone deactelyases and the histone methyltransferase, EZH2, could impede epithelial differentiation and contribute to prostate cancer progression, in part through modulating the transcriptional output of AR. Gene expression profiling of human prostate cancer VCaP cells with time course DHT stimulation using microarray.
2012-04-26 | E-GEOD-35540 | biostudies-arrayexpress
Project description:Deregulation of the Androgen Receptor (AR) transcriptional network is a common hallmark in prostate cancers. To achieve its precise transcriptional role, AR needs to co-operate specifically with a plethora of cofactors. In prostate cancers, AR transcription collaborators are frequently aberrantly over-expressed, altering the AR signaling pathway to one that promotes oncogenesis. Recently, the prostate cancer recurrent fusion gene, ERG, was shown to promote tumor progression by acting as a repressor of AR signaling. However, the exact mechanics and the functional consequences associated with this crosstalk between ERG and AR still remains relatively unknown. Interestingly, through chromatin immunoprecipitation coupled with massively parallel sequencing, we discover that ERG and other commonly over-expressed transcriptional co-repressors (HDAC1, HDAC2, HDAC3 and EZH2) are wired into an AR-centric transcriptional network via a spectrum of distal enhancers and/or proximal promoters. We show that ERG represses several AR target genes involved in epithelial differentiation. Furthermore, we demonstrated that suppression of the androgen-induced gene, Vinculin, by ERG and histone deacetylases increases cancer cell invasiveness. From our results, we propose that ERG, histone deactelyases and the histone methyltransferase, EZH2, could impede epithelial differentiation and contribute to prostate cancer progression, in part through modulating the transcriptional output of AR. Gene expression profiling of human prostate cancer VCaP cells with time-course dihydrotestosterone (DHT) stimulation using microarrays. Triplicates were generated for each treatment/time point.
2012-04-26 | E-GEOD-28948 | biostudies-arrayexpress
Project description:Chromosomal rearrangements involving ETS factors, ERG and ETV1, occur frequently in prostate cancer. We here examine human prostate cancer cells control VCaP and LNCaP cells with ERG- or ETV1-silenced VCaP or LNCaP cells, respectively, in hormone deprived and stimulated conditions. VCAP and LNCaP cells, 24 hr after ERG or ETV1 RNA interference, respectively, were grown in hormone-depleted conditions for 2 days, and then in the presence of EtOH (vehicle) or 10nM DHT for 16hr. Total RNA was extracted from three biological replicates. This was used to hybridize to Affymetrix expression arrays using the HG-U133 Plus 2.0 platform.
2013-03-01 | E-GEOD-39354 | biostudies-arrayexpress
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