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Updated: Mar 7, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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Aurora A regulates expression of AR-V7 in models of castrate resistant prostate cancer

Dominic Jones1, Martin Noble1, Steve R Wedge1

  • 1Northern Institute for Cancer Research, Newcastle University, Paul O'Gorman Building, Framlington Place, Newcastle upon Tyne, Ne2 4HH, UK.

Scientific Reports
|February 17, 2017
PubMed

Insights

Aurora A kinase regulates androgen receptor variants (AR-Vs) in prostate cancer. Inhibiting Aurora A reduces AR-V7 expression and CRPC cell growth, suggesting it as a therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Androgen receptor variants (AR-Vs) are key drivers of therapy evasion in castrate-resistant prostate cancer (CRPC).
  • Mechanisms regulating AR-V expression and their role in CRPC progression are not fully understood.

Purpose of the Study:

  • To investigate the role of Aurora A kinase in the regulation of AR-Vs in CRPC models.
  • To determine if Aurora A inhibition can impact AR-V expression and CRPC cell viability.

Main Methods:

  • Depletion and inhibition of Aurora A kinase in CRPC models.
  • Analysis of AR pre-mRNA splicing and AR-V transcript levels.
  • Assessment of AR-V target gene expression, CRPC cell proliferation, and survival.

Main Results:

  • Aurora A kinase depletion reduces AR-V target gene expression and AR-V-driven proliferation and survival.
  • Aurora A kinase knockdown specifically alters AR pre-mRNA splicing to down-regulate AR-V synthesis, including AR-V7, without affecting full-length AR mRNA.
  • Aurora A inhibition reproduces these effects, and AURKA is identified as an AR-V target gene, indicating a positive feedback loop.

Conclusions:

  • Aurora A kinase plays a critical role in regulating AR-V expression, particularly AR-V7, in CRPC.
  • Targeting Aurora A kinase represents a promising therapeutic strategy for CRPC by disrupting AR-V signaling and promoting cell death.

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