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Genome-wide maps of H3K4me2/3 in prostate cancer cell line LNCaP

ABSTRACT: We report the high-throughput profiling of histone modifications in prostate cancer cells. By obtaining over 1 billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of prostate cancer cells. we found androgen treatment dismisses a nucleosome over AR binding sites that are flanked by a pair of H3K4me2 marked nucleosomes. A novel quantitative model built on the behavior of such nucleosome pairs correctly identified regions bound by the regulators of the immediate androgen response including AR and FoxA1. More importantly this model also correctly predicted novel binding sites for other transcription factors present following prolonged androgen stimulation including Oct1 and NKX3.1. Thus quantitative modeling of enhancer structure provides a powerful predictive method to infer the identity of transcription factors involved in cellular responses to specific stimuli.

ORGANISM(S): Homo sapiens

PROVIDER: GSE20042 | GEO | 2010/03/09

SECONDARY ACCESSION(S): PRJNA124303

REPOSITORIES: GEO

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Genome-wide maps of H3K4me2/3 in prostate cancer cell line LNCaP

Project description:We report the high-throughput profiling of histone modifications in prostate cancer cells. By obtaining over 1 billion bases of sequence from chromatin immunoprecipitated DNA, we generated genome-wide chromatin-state maps of prostate cancer cells. we found androgen treatment dismisses a nucleosome over AR binding sites that are flanked by a pair of H3K4me2 marked nucleosomes. A novel quantitative model built on the behavior of such nucleosome pairs correctly identified regions bound by the regulators of the immediate androgen response including AR and FoxA1. More importantly this model also correctly predicted novel binding sites for other transcription factors present following prolonged androgen stimulation including Oct1 and NKX3.1. Thus quantitative modeling of enhancer structure provides a powerful predictive method to infer the identity of transcription factors involved in cellular responses to specific stimuli. Examination of 2 different histone modifications in prostate cancer cells with and without androgen (dihydrotestosterone, DHT) treatment.

2010-03-09 | E-GEOD-20042 | biostudies-arrayexpress

Effects of Oct1 inhibition in AR signaling

Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. Oct1 is an AR interacting partner and regulates the transcriptional activity of AR. In order to investigate the Oct1 function in prostate cancer cells, we performed gene expression in AR-positive prostate cancer cell lines after siOct1 or pyrrole-imidazole (PI) polyamide targeting Oct1-binding treatment. We also treated cells with vehicle or androgen to analyze the effects of Oct1 on AR function. Observation of androgen dependent gene expression changes after treatment with siOct1 or polyamide targeting Oct1 with microarray.

2016-04-01 | E-GEOD-77650 | biostudies-arrayexpress

Effects of Oct1 inhibition in AR signaling

2016-04-01 | GSE77650 | GEO

Genome-wide maps of chromatin state in patient-derived model (PDX) of AR-positive or negative CRPC

Project description:We investigated the global OCT1 genomic signals using high-throughput chromatin immunoprecipitation sequencing (ChIP-seq) in a patient-derived model (PDX) of androgen receptor (AR)-negative or positive castration resistant prostate cancer (CRPC).

2022-04-20 | GSE193073 | GEO

Effects of OCT1 knockdown in castration-resistant prostate cancer cells

Project description:Prostate cancer is the most common cancer in men and AR downstream signalings promote prostate cancer cell proliferation. Although initially hormone-deprovation therapy is effective to inhibit cancer progression, most of cancers relapse as castration-resistant prostate cancer (CRPC). Therefore, we examined the effect of AR interacting partner OCT1 in CRPC cells. In order to investigate the OCT1 function in CRPC cells, we performed gene expression in AR-positive CRPC cell line, 22Rv1, after siOCT1 treatment. We also treated cells with vehicle or dihydrotestosterone (DHT) to analyzed the effects of OCT1 on AR function.

2019-03-01 | GSE123517 | GEO

Spermine is a natural suppressor of AR signaling in castration-resistant prostate cancer

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

A computational systems approach for identification of synergistic specification genes facilitates lineage conversion to prostate tissue

Project description:We report that a computational systems approach can identify cell type specification genes that act synergistically, and demonstrate its application for reprogramming of fibroblasts to prostate tissue. We have employed three such master regulators (FOXA1, NKX3.1, and androgen receptor, AR) in a primed conversion strategy to generate prostate tissue from mouse fibroblasts, involving expression of pluripotency factors, tissue recombination with embryonic urogenital mesenchyme, and renal grafting.

2017-04-21 | GSE83298 | GEO

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

Genome-wide maps of H3K4me2 and DNase I hypersensitivity sites in prostate cancer cell line LNCaP and breast cancer cell line MCF-7.

Project description:We report the high-throughput profiling of histone modification and DNase I hypersensitivity sites in prostate cancer and breaset cancer cells. We found that while AR binding is associated with nucleosome depletion, ER binding is not. We showed that a quantitative measure of DNase I hypersensitivity changes is a powerful tool in indentifying transcription factor cistromes. Examination of histone modification marked nucleosomes and Dnase I hypersensitivity in prostate cancer and breast cancer cells with and without hormone treatment.

2012-03-25 | E-GEOD-33216 | biostudies-arrayexpress

Genome-wide maps of H3K4me2 and DNase I hypersensitivity sites in prostate cancer cell line LNCaP and breast cancer cell line MCF-7.

2012-03-25 | GSE33216 | GEO

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