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

ABSTRACT: 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).

ORGANISM(S): Homo sapiens

PROVIDER: GSE76141 | GEO | 2015/12/19

SECONDARY ACCESSION(S): PRJNA306425

REPOSITORIES: GEO

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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

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Project description:Elevated levels of androgen receptor (AR) in prostate cancer confer resistance to current antiandrogens and play a causal role in disease progression due to persistent target gene activation. Through pharmacologic and genetic approaches, we show that half of all direct AR target genes, including TMPRSS2, the primary driver of ETS fusion transcripts in 70 percent of human prostate cancers, require histone deacetylase (HDAC) activity for transcriptional activation by AR. Surprisingly, the HDAC3-NCoR complex, which typically functions to repress gene expression by nuclear receptors, is required for AR target gene activation. Prostate cancer cells treated with HDAC inhibitors have reduced AR protein levels, but we show that the mechanism of blockade of AR activity is through failure to assemble a coactivator/RNA polymerase II complex after AR binds to the enhancers of target genes. Failed complex assembly is associated with a phase shift in the cyclical wave of AR recruitment that typically occurs in response to ligand treatment. HDAC inhibitors retain the ability to block AR activity in hormone refractory prostate cancer models and therefore merit clinical investigation in this setting. HDAC-regulated AR target genes defined here can serve as biomarkers to ensure sufficient levels of HDAC inhibition. Experiment Overall Design: LNCaP prostate cancer cells were grown in charcoal stripped, androgen deplete medium. They were then stimulated with or without 1nM R1881 and with or without two doses of HDAC inhibitors TSA, SAHA, and LBH 589. Cyclohexamide was include to block new protein synthesis. Cells were harvested 16 hours after treatment.

2009-01-09 | E-GEOD-9000 | biostudies-arrayexpress

shRNA profiling of human luciferase (ctrl), HDAC1, HDAC2, and HDAC8 LnCAP cells were generated to examine the effect of individual HDAC knockdown on expression of androgen induced genes

Project description:Elevated levels of androgen receptor (AR) in prostate cancer confer resistance to current antiandrogens and play a causal role in disease progression due to persistent target gene activation. Through pharmacologic and genetic approaches, we show that half of all direct AR target genes, including TMPRSS2, the primary driver of ETS fusion transcripts in 70 percent of human prostate cancers, require histone deacetylase (HDAC) activity for transcriptional activation by AR. Surprisingly, the HDAC3-NCoR complex, which typically functions to repress gene expression by nuclear receptors, is required for AR target gene activation. Prostate cancer cells treated with HDAC inhibitors have reduced AR protein levels, but we show that the mechanism of blockade of AR activity is through failure to assemble a coactivator/RNA polymerase II complex after AR binds to the enhancers of target genes. Failed complex assembly is associated with a phase shift in the cyclical wave of AR recruitment that typically occurs in response to ligand treatment. HDAC inhibitors retain the ability to block AR activity in hormone refractory prostate cancer models and therefore merit clinical investigation in this setting. HDAC-regulated AR target genes defined here can serve as biomarkers to ensure sufficient levels of HDAC inhibition. Experiment Overall Design: Lentiviral shRNA mediated knockdown of Luciferase (ctrl), HDAC1, HDAC2, and HDAC8 LnCAP cells were generated. They were grown in charcoal stripped, androgen deplete medium. They were then stimulated with or without 1nM R1881. Cyclohexamide was include to block new protein synthesis. Cells were harvested 16 hours after treatment.

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Time course of androgen-regulated transcripts in LNCaP cells

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DHT (androgen) effect on the gene expression of LNCaP cell line

Project description:Androgen receptor (AR) is essential for the development and progression of prostate cancer (PCa), but the exact role of AR in these processes remains unclear. To examine the direct effect of AR signaling on gene transcription, the cells were perfused with charcoal-dextran stripped fetal bovine serum (CD-FBS) for 3 days, and then treated with 10 nM dihydrotestosterone (DHT) for 24 hours. Deep sequencing of rRNA-depleted total RNAs was performed in biological duplicates on LNCaP cells.

2021-01-18 | GSE163539 | GEO

Expression data from LNCaP cell line

Project description:Androgen receptor (AR) is a ligand-dependent transcription factor that plays a key role in the onset and progression of prostate cancer. Surprisingly little is known of AR binding sites and collaborating transcription factors in the human genome. Here we have identified the DNA sequence motifs that are significantly enriched within the authentic 90 AR target regions found on chromosomes 21 and 22 in human prostate cancer cells by combining chromatin immunoprecipitation for AR with chromosome-scale tiled oligonucleotide microarrays. By integrating the DNA sequence motif data with the gene expression profiles from human prostate cancers we identified the transcription factors that recognize each of these motifs. These factors form complexes with AR, bind to specific AR target regions and govern androgen-dependent transcription. Together with AR these collaborating transcription factors form a regulatory network that directs prostate cancer growth and survival and identify potential new opportunities for therapeutic intervention. Keywords: time course

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