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Updated: Feb 9, 2026

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer
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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

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Diverse AR-V7 cistromes in castration-resistant prostate cancer are governed by HoxB13

Zhong Chen1,2, Dayong Wu3, Jennifer M Thomas-Ahner4

  • 1Department of Pathology, Duke University School of Medicine, Durham, NC 27710.

Proceedings of the National Academy of Sciences of the United States of America
|May 31, 2018
PubMed

Insights

Androgen receptor splice variant 7 (AR-V7) drives castration-resistant prostate cancer (CRPC). HoxB13 protein is essential for AR-V7’s genomic function and promotes CRPC growth, suggesting HoxB13 as a potential therapeutic target.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genomics

Background:

  • The androgen receptor splice variant 7 (AR-V7) is crucial for castration-resistant prostate cancer (CRPC) progression.
  • The precise genomic mechanisms by which AR-V7 drives CRPC remain largely unelucidated.

Purpose of the Study:

  • To investigate the genomic binding patterns and functional role of AR-V7 in CRPC.
  • To identify key regulators of AR-V7's transcriptional activity in CRPC.

Main Methods:

  • Chromatin immunoprecipitation followed by exonuclease digestion (ChIP-exo) was employed to map AR-V7 binding sites.
  • CRPC cell lines and patient tissues were analyzed for AR-V7 and HoxB13 interactions.
  • CRPC cell growth was assessed following HoxB13 silencing.

Main Results:

  • AR-V7 binds to distinct genomic regions, recognizing androgen-responsive elements in CRPC cells and tissues.
  • AR-V7 cistromes exhibit significant variability across different CRPC contexts, affecting diverse gene sets.
  • HoxB13 is universally required for AR-V7 binding, physically interacts with AR-V7, and co-regulates oncogene expression.
  • HoxB13 silencing inhibits AR-V7's oncogenic function and reduces CRPC growth.

Conclusions:

  • HoxB13 acts as a critical upstream regulator of AR-V7-driven transcriptomes in a context-dependent manner in CRPC.
  • HoxB13 is a potential therapeutic target for AR-V7-positive prostate tumors.
Keywords:
AR-V7HoxB13castration-resistant prostate cancermotif-resolution cistromes

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