Related Experiment Video

Updated: Nov 21, 2025

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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The role of JMJD6/U2AF65/AR-V7 axis in castration-resistant prostate cancer progression

Dali Tong1

  • 1Department of Urology, Daping Hospital, Army Medical University, Chongqing, People's Republic of China. tongdali1985@163.com.

Cancer Cell International
|January 12, 2021
PubMed

Insights

JMJD6 enzyme promotes androgen receptor (AR) transcription and AR-V7 splicing in castration-resistant prostate cancer (CRPC) via a novel JMJD6/U2AF65/AR-V7 axis, offering new therapeutic targets.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Castration-resistant prostate cancer (CRPC) is a major challenge in prostate cancer treatment.
  • Abnormal androgen receptor (AR) activation, particularly AR-V7 splicing, is a key driver in CRPC progression.
  • The precise regulation of AR-V7 mRNA splicing remains incompletely understood.

Purpose of the Study:

  • To propose a novel mechanism for AR mRNA splicing in CRPC progression.
  • To elucidate the role of the dual-function enzyme JMJD6 in regulating AR mRNA transcription and splicing.
  • To investigate the potential JMJD6/U2AF65/AR-V7 axis in CRPC.

Main Methods:

  • Hypothesis-driven research exploring enzyme functions in mRNA regulation.
  • Focus on JMJD6's demethylase and hydroxylase activities.
  • Investigation of JMJD6's interaction with U2AF65 and the AR gene.

Main Results:

  • JMJD6 is hypothesized to promote AR mRNA transcription via demethylation of H3R/H4R at the AR promoter.
  • JMJD6 is proposed to interact with U2AF65, facilitating AR-V7 splicing through its hydroxylase activity.
  • The novel JMJD6/U2AF65/AR-V7 axis is implicated in CRPC progression.

Conclusions:

  • JMJD6 plays a potential dual role in both AR transcription and AR-V7 splicing.
  • The proposed JMJD6/U2AF65/AR-V7 axis offers a new perspective on CRPC pathogenesis.
  • Targeting JMJD6 may represent a novel therapeutic strategy for CRPC.

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