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62 reviewsSUMMARYContinued reliance on the androgen receptor (AR) after androgen deprivation therapy (ADT) fails causes35,000 American prostate cancer (CaP) deaths annually. Targeting the AR’s transcriptional activity couldovercome this acquired resistance, but has been challenging. We demonstrate the therapeutic potential ofdisrupting interactions between the AR and its coregulator WDR77. WDR77 stimulated CaP growth, andits overexpression was associated with worse patient survival. AR and WDR77 cistromes overlapped considerably, and AR- and WDR77-bound genes correlated with aggressive CaP features. Direct WDR77-AR interaction occurred, which, when disrupted, prevented AR-WDR77 complex formation, reduced AR DNA-binding and AR-dependent gene expression, and decreased cell proliferation to the same extent as ADT. Suchinterference inhibited cell growth by ADT-resistant AR action and after ADT-resistance without impactingAR-negative CaP or benign cells. Blocking AR-WDR77 cooperation also delayed the growth of organoidsfrom patient-derived xenografts and fresh CaP specimens. Disrupting coregulator control over AR actionmay thus improve survival from ADT-resistant CaP.
