ArticleCell reports2025
Disrupting the interaction between androgen receptor and its coregulator WDR77 delays the growth of treatment-resistant prostate cancer.
Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Emerging hallmarks and the rise of complexities and heterogeneity of tumor.Biochemistry and biophysics reports · 2025Review
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Authors and funding
17 authors.
Funding
Abstract
Continued reliance on the androgen receptor (AR) after androgen deprivation therapy (ADT) fails causes 35,000 American prostate cancer (CaP) deaths annually. Targeting the AR's transcriptional activity could overcome this acquired resistance, but has been challenging. We demonstrate the therapeutic potential of disrupting interactions between the AR and its coregulator WDR77. WDR77 stimulated CaP growth, and its 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. Such interference inhibited cell growth by ADT-resistant AR action and after ADT-resistance without impacting AR-negative CaP or benign cells. Blocking AR-WDR77 cooperation also delayed the growth of organoids from patient-derived xenografts and fresh CaP specimens. Disrupting coregulator control over AR action may thus improve survival from ADT-resistant CaP.
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