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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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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

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

2016-03-01 | GSE66977 | GEO

PIAS1 is a target gene selective androgen receptor coregulator in prostate cancer cell chromatin

Project description:To study the importance of PIAS1 (protein inhibitor of activated STAT1) for the androgen-regulated transcriptome of VCaP prostate cancer cells, we silenced its expression by RNAi. Transcriptome analyses revealed that a subset of the androgen-regulated genes is significantly influenced, either activated or repressed, by PIAS1 depletion. The depletion also exposed a completely new set of genes to androgen regulation, suggesting that PIAS1 can mask genes from androgen receptor (AR). Pathway analyses of gene expression data suggest involvement of PIAS1 in VCaP cell proliferation. According to genome-wide ChIP-seq analyses, PIAS1 interacts with the AR on chromatin harboring also SUMO2/3, as androgen exposure multiplied the occupancy of PIAS1 in the chromatin, and resulted in nearly complete overlap with AR chromatin binding events. PIAS1 interacted also with pioneer factor FOXA1 in the chromatin. Our results strongly suggest that PIAS1 is a genuine chromatin-bound coregulator of AR which functions in a target gene selective fashion in prostate cancer cells.

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Project description:CRISPR was utilized to deplete either PRMT5 or WDR77 in HSC-5 cells. Subsequently, RNA-seq was performed to identify changes in the transcriptome following the loss of PRMT5 or WDR77 in these cells. Critically, Gene Set Enrichment Analysis (GSEA) was conducted to screen and identify a list of genes co-regulated by PRMT5 and WDR77.

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ERG-mediated coregulator complex formation maintains androgen receptor signaling in prostate cancer

Project description:ERG-mediated coregulator complex formation maintains androgen receptor signaling in prostate cancer

| PRJNA661225 | ENA