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Effect of p53 knowkdown on genome-wide map of AR-DNA binding

ABSTRACT: We report that p53 knockdown changed AR-DNA binding across the genome. We found fewer AR-binding sites in the absence of p53.

ORGANISM(S): Homo sapiens

PROVIDER: GSE31294 | GEO | 2012/07/31

SECONDARY ACCESSION(S): PRJNA146107

REPOSITORIES: GEO

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Effect of p53 knowkdown on genome-wide map of AR-DNA binding

Project description:We report that p53 knockdown changed AR-DNA binding across the genome. We found fewer AR-binding sites in the absence of p53. Examination of AR-DNA binding after p53 knockdown in LNCaP cells

2012-07-31 | E-GEOD-31294 | biostudies-arrayexpress

Effect of FOXA1 over-expression upon AR binding in AR-driven cancers

Project description:Effect of FOXA1 over-expression upon AR binding in AR-driven cancers

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Next Generation Sequencing Facilitates Quantitative Analysis of effect of knockdown of GATA2 on AR binding sites

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to compare AR binding activity in LNCaP cells with and without knockdown of GATA2. Methods: LNCaP cells between passage number 32-34 were used for assay. Cells are transfected with GATA2 specific or nonspecific siRNA and ChIP was performed, the ChIP producted was further used to generate library with illumina ChIP-seq kit. Hi-seq 2500 was used for sequencing and the data was analyzed by MACs for peaks. Results: GATA2 knockdown lead to changes of AR binding activity , in most AR binding sites, AR shows decreased bindig activity. Only small percent sites show increased binding. Conclusions: Our study represents the first detailed analysis of the relationship between GATA2 and AR binding in whole genomic DNA.These results demostrate GATA2 play a critical role in AR activity in prostate cancer. LNCaP cells was used as cell model were treated with specific GATA2 siRNA.Library was sequenced using Illumina HI-seq 2500.

2014-01-21 | E-GEOD-52725 | biostudies-arrayexpress

Effect of FOXA1 over-expression upon AR binding in AR-driven cancers

Project description:We performed androgen receptor (AR) ChIP-seq after GFP control or FOXA1 over-expression in two AR driven cancer models; LNCaP prostate cancer cell line and MDA-MB-453 molecular apocrine breast cancer cell line.

2014-01-14 | E-MTAB-1749 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of effect of knockdown of GATA2 on AR binding sites

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Coupling p53 binding and nucleosome occupancy measurements at p53 binding sites

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Coupling p53 binding and nucleosome occupancy measurements at p53 binding sites

Project description:We were interested to explain why p53 binds some high affinity sites in contrast to other high affinity sites that are not bound by p53. p53 binding was measured using p53 ChIP-CHIP and in parallel nucleosome occupancy was measured on these same sites Comparison between p53 binding and nucleosome occupancy at p53 predicted binding sites ChIP-CHIP of p53 from MCF7EcoR under Basal conditions and MCF7EcoR treated with NCS (Activated) and Mononucleosomal extraction from MCF7sip53, MCF7EcoR under Basal conditions and MCF7EcoR treated with NCS (Activated) Expression analysis of MCF7sip53 and MCF7EcoR treated with NCS (Activated)

2010-08-09 | E-GEOD-22783 | 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

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.

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identifying all AR binding regions in PC346C cell line

Project description:The Androgen Receptor plays in general an important role in Prostate Cancer biology. The Androgen Receptor orchestrates as transcription factor the activity of AR-regulated genes at destinct genomic regions by binding to specific sequences (known as Androgen Responsive Elements - ARE). However, the biophysical nature of the Androgen Receptor at these binding sites on the DNA are not well characterized. In order to investigate the biophysical properties of these molecules at AR binding sites by super resolution microscopy in living cells, we performed a AR-ChIP sequencing for the PC346C target cell line. Based on the sequencing results, we selected certain target regions based on relative AR-enrichment for further studying the local AR dynamics in these target regions.

2023-09-18 | GSE229728 | GEO

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