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The impact of WDR77 on the AR cistrome in prostate cancer cells

ABSTRACT: The impact of WDR77 on the AR cistrome in prostate cancer cells

PROVIDER: PRJNA1063602 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27496310_1.fastq.gz	Fastqsanger.gz
	SRR27496310_2.fastq.gz	Fastqsanger.gz
	SRR27496311_1.fastq.gz	Fastqsanger.gz
	SRR27496311_2.fastq.gz	Fastqsanger.gz
	SRR27496312_1.fastq.gz	Fastqsanger.gz

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The impact of WDR77 on the AR cistrome in prostate cancer cells

Project description:Androgen receptor (AR) drives prostate cancer (CaP) even after androgen deprivation therapy (ADT) failed. Inhibiting AR’s transcription factor function to overcome acquired resistance to ADT is an attractive therapeutic avenue. However, which AR-coregulator interaction should be targeted is not clear, AR-coregulator complex higher order structures and stoichiometry are unknown, and how manipulating AR-coregulator interactions impacts the AR cistrome is not understood. Here, we examine interactions between AR and WD repeat 77 (WDR77, non-catalytic component of the methylosome complex), which are enriched in ADT-resistant CaP and mediate CaP cell survival. We performed CUT&RUN assays defined AR and WDR77 cistromes, the WDR77-dependence of the AR cistrome and the overlap between the AR and WDR77 cistromes in CaP cells.

2025-01-10 | GSE252993 | GEO

Disrupting the interaction between androgen receptor and its coregulator WDR77 delays the growth of treatment-resistant prostate cancer

Project description:Continued reliance on androgen receptor (AR) after androgen deprivation therapy (ADT) has failed causes 35,000 American prostate cancer (CaP) deaths annually. AR’s transcriptional activity is an attractive target to overcome this acquired resistance but has been challenging to pursue. We demonstrate the therapeutic potential of disrupting interactions between AR and its coregulator WDR77. WDR77 stimulated growth of CaP cells and xenografts and its overexpression associated with worse patient survival. AR and WDR77 cistromes overlapped considerably, AR- and WDR77-bound genes correlated with aggressive CaP features, and the AR cistrome was reduced after WDR77 loss. We delineated direct interaction between WDR77 and AR, which when disrupted prevented AR-WDR77 complex formation, reduced AR DNA-binding and AR-dependent gene expression. Such disruption decreased cell proliferation to the same extent as ADT, and inhibited cell growth when ADT-resistant AR action was modelled and after ADT-resistance without impacting AR-negative CaP cells or benign cells. Blocking AR-WDR77 cooperation also delayed growth of organoids generated from patient-derived xenografts and fresh CaP specimens. Disrupting coregulator control over AR action may thus improve survival from ADT-resistant CaP.

2025-03-24 | GSE287925 | GEO

Cistrome analyses of AR stimulated by 0.1 nM DHT in LNCaP stable cell line overexpressing AR [ChIP-Seq]

Project description:The molecular drivers for the AR signaling reprogramming in castration-resistant prostate cancer remain to be determined. In this study, we hypothesize that increased AR expression in conjunction with lower-level androgens, which is a typical condition in prostate cancer cells receiving androgen deprivation therapy, is a major driving force of the reprogramming. To test this, we used LNCaP model with inducible overexpression of AR to examine the acute effects of AR overexpression stimulated by low-dose DHT (0.1nM) on AR cistrome.

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Cistrome analyses of AR-V7.

Project description:Cistrome analyses of AR-V7.

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Genome-wide analysis of genes regulated by p44/wdr77 and PRMT5 in lung and prostate cancer cells

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Contribution of WDR77 and p53 to androgen response in prostate cancer cells

Project description:To decipher the contribution of WDR77 and p53 to androgen-responsive gene expression, effect of siRNA-mediated silencing of WDR77 and p53 on expression of androgen-dependent genes was studied. Human LNCaP prostate cancer cells were transfected with individual siRNA SmartPools targeting WDR77 or p53 or a non-targeting siRNA SmartPool. Forty-two hours after transfection, cells were treated with synthetic androgen R1881 (5nM) or vehicle. Three biological replicates were generated per treatment group. Forty-eight hours later, total RNA was isolated and processed for Illumina oligoarray analysis.

2016-03-01 | E-GEOD-66977 | biostudies-arrayexpress

Genome-wide analysis of genes regulated by p44/wdr77 and PRMT5 in lung and prostate cancer cells

2014-04-14 | GSE56757 | GEO

The cistrome and transcriptome landscape of androgen receptor splice variants in castration-resistant prostate cancer cells

Project description:The spliced variant forms of androgen receptor (AR-Vs) have been identified recently in castration-resistant prostate cancer (CRPC) cell lines and clinical samples. Here we identified the cistrome and transcriptome landscape of AR-Vs in CRPC cell lines and determine the clinical significance of AR variants regulated gene.The AR variants binding sites can be identified in 22Rv1 cell line in the absence of androgen. Knocking down full-length AR (AR-FL) doesn't affect AR-Vs binding sites in genome-wide. A set of genes were identified to be regulated uniquely by AR-Vs, but not by AR-FL in androgen-depleted condition. Integrated analysis showed that some genes may be modulated by AR-Vs directly. Unsupervised clustering analysis demonstrated that AR variants gene signature can separate not only the benign and malignant prostate tissue, but also the localized prostate cancer and metastatic CRPC specimens. Some genes modulated uniquely by AR variants were also identified to correlate with the Gleason Pattern of prostate cancer and PSA failure. We conclude that AR spliced variants bind to DNA independent of full-length AR, and can modulate a unique set of genes which is not regulated by full-length AR in the absence of androgen. AR variants gene signature correlate with CRPC and prostate cnacer disease progress. Androgen receptor (AR) binding sites in human prostate cancer 22Rv1 cell lines were studied using ChIP-seq. ChIP enriched and input DNA were sequenced using Illumina HiSeq 2000.

2014-09-10 | E-GEOD-58478 | 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.

2023-10-11 | MTBLS8034 | MetaboLights

An AR-ERG co-mediated chromatin interactome defines the transcriptional network in prostate cancer cells

Project description:An aberrant androgen receptor (AR) transcriptional network underpins prostate cancer development. Even though the AR cistrome had been extensively studied in prostate cancers, information pertaining to the spatial architecture of the AR transcriptional circuitry remains limited due to the absence of an AR-associated chromatin interactome map. To resolve this, we utilized chromatin interaction analysis by paired-end tag (ChIA-PET) sequencing to profile AR-associated and ERG-associated long range chromatin interactions in an ERG fusion positive prostate cancer cell line. We identified ERG-associated long range chromatin interactions as an elemental component in the AR-associated chromatin interactome, acting in concert, to achieve coordinated regulation of AR target genes. In addition, we characterized the epigenetic signature of the AR/ERG anchor binding sites and implicated AR and ERG associated chromatin loopings for facilitating fusion gene formation in prostate cancers. Taken together, our results revealed the presence of an AR/ERG defined higher order chromatin structure exploited for driving prostate cancer progression.

2018-12-14 | GSE54946 | GEO

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