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

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

PROVIDER: PRJNA1215293 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR32109332_1.fastq.gz	Fastqsanger.gz
	SRR32109332_2.fastq.gz	Fastqsanger.gz
	SRR32109333_1.fastq.gz	Fastqsanger.gz
	SRR32109333_2.fastq.gz	Fastqsanger.gz
	SRR32109334_1.fastq.gz	Fastqsanger.gz

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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

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.

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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.

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Project description:Comprehensive RNA-seq experiments in control and PRMT5 and WDR77 shRNA infected cells delineate the role of PRMT5/WDR77 complex in promoting breast cancer oncogenesis

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Project description:Analysis of gene expression in lung and prostate cancer cells expressing non-target (NT), p44/wdr77. or PRMT5 shRNA. Results provide important information on how p44/wdr77 and PRMT5 control cellular proliferation. Total RNA obtained from cells expressing NT, p44/wdr77, or PRMT5 shRNA.

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