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Updated: Apr 30, 2026

Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients
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Sequencing Small Non-coding RNA from Formalin-fixed Tissues and Serum-derived Exosomes from Castration-resistant Prostate Cancer Patients

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The link between androgen receptor splice variants and castration-resistant prostate cancer

Cynthia C T Sprenger1, Stephen R Plymate

  • 1Department of Medicine, University of Washington, Seattle, WA, 98104, USA, cts2501@u.washington.edu.

Hormones & Cancer
|May 7, 2014
PubMed

Insights

Androgen receptor splice variants (AR-Vs) drive resistance to advanced prostate cancer therapies like abiraterone and enzalutamide. Understanding AR-V mechanisms is crucial for developing new treatments for castration-resistant prostate cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Advanced prostate cancer treatments, including abiraterone and enzalutamide, face resistance.
  • Increased expression of androgen receptor splice variants (AR-Vs) is linked to this therapy resistance.

Purpose of the Study:

  • To review the role of androgen receptor splice variants (AR-Vs) in prostate cancer therapy resistance.
  • To explore potential mechanisms leading to AR-V expression and their impact on treatment efficacy.

Main Methods:

  • Literature review of studies on androgen receptor signaling in prostate cancer.
  • Analysis of mechanisms underlying resistance to androgen receptor-directed therapies.
  • Examination of the role of AR-Vs in castration-resistant prostate cancer.

Main Results:

  • Androgen receptor splice variants (AR-Vs) are associated with resistance to abiraterone and enzalutamide.
  • Genomic rearrangement and alternative splicing of AR pre-mRNA are potential mechanisms for AR-V formation.
  • Therapy bypass mechanisms can vary, complicating treatment strategies.

Conclusions:

  • Androgen receptor splice variants (AR-Vs) represent a significant mechanism of resistance in advanced prostate cancer.
  • Further research is needed to elucidate the precise mechanisms of AR-V generation and their clinical implications.
  • Determining whether AR-V-driven or AR-independent pathways dominate castration-resistant disease is critical for future therapeutic development.

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