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Reprogramming of Androgen Receptor Activity in Castration-resistant Prostate Cancer is Shaped by Truncated Variants.

Mitchell G Lawrence1, Shivakumar Keerthikumar2, Scott L Townley3

  • 1Department of Anatomy and Developmental Biology, Biomedicine Discovery Institute, Monash University, Clayton, Australia; Peter MacCallum Cancer Centre, Melbourne, Australia; Sir Peter MacCallum Department of Oncology, University of Melbourne, Melbourne, Australia; Cabrini Institute, Cabrini Health, Malvern, Australia; Melbourne Urological Research Alliance, Monash University, Clayton, Australia.

European Urology Focus
|April 12, 2025
PubMed
Summary

Androgen receptor (AR) variants like ARv567es drive prostate cancer therapy resistance by altering gene expression. Identifying ARv567es may help guide treatment decisions for resistant prostate cancer.

Keywords:
Androgen deprivation therapyAndrogen receptorBipolar androgen therapyChromatin immunoprecipitationCistromePatient-derived xenograftProstate cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer cells develop constitutively active androgen receptor (AR) variants under treatment pressure.
  • The role of AR variants in therapy resistance is debated due to coexpression with full-length AR.

Purpose of the Study:

  • To investigate how AR variants influence AR chromatin occupancy and treatment responses.
  • To differentiate the effects of AR variants in the presence and absence of full-length AR.

Main Methods:

  • Utilized patient-derived xenografts of metastatic prostate cancer with diverse AR alterations.
  • Employed chromatin immunoprecipitation and RNA sequencing to analyze AR binding and transcriptomic profiles.
  • Assessed treatment responses to castration and bipolar androgen therapy in mouse models.

Main Results:

  • Identified a distinct tumor group characterized by ARv567es expression, resulting from AR gene rearrangements.
  • ARv567es-positive tumors exhibited unique epigenomic and transcriptional profiles, including altered AR-regulated and AR-repressed genes.
  • These tumors demonstrated resistance to castration and bipolar androgen therapy, with dampened transcriptional responses and disrupted AR autoregulation when coexpressing full-length AR.

Conclusions:

  • ARv567es emergence through gene rearrangements induces transcriptional reprogramming and confers therapy resistance in prostate cancer.
  • ARv567es serves as a potential biomarker for guiding treatment strategies in advanced prostate cancer.