Related Experiment Video

Updated: Jul 9, 2025

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors
06:07

Continuous Fluorescence-Based Endonuclease-Coupled DNA Methylation Assay to Screen for DNA Methyltransferase Inhibitors

Published on: August 5, 2022

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Methylation of the epigenetic JMJD2D protein by SET7/9 promotes prostate tumorigenesis

Ruicai Gu1, Tae-Dong Kim1, Hanlin Jiang2

  • 1Department of Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK, United States.

Frontiers in Oncology
|December 4, 2023
PubMed

Insights

JMJD2D epigenetic regulator overexpression fuels prostate cancer growth. Lysine methylation of JMJD2D impacts cancer cell behavior and influences CBLC gene expression, highlighting potential therapeutic targets for prostate cancer treatment.

Area of Science:

  • Epigenetics
  • Molecular Oncology
  • Biochemistry

Background:

  • The role of the JMJD2D epigenetic regulator in prostate cancer remains unclear.
  • Understanding JMJD2D regulation is crucial for identifying new therapeutic strategies.

Purpose of the Study:

  • To investigate the regulation and function of JMJD2D in prostate cancer.
  • To elucidate the downstream effects of JMJD2D activity on cancer progression.

Main Methods:

  • Analysis of JMJD2D expression in prostate tumors.
  • Site-directed mutagenesis of JMJD2D at K427.
  • Cell growth, invasion, and tumor formation assays.
  • Transcriptomic analysis.
  • Bioinformatic analyses of gene expression.

Main Results:

  • JMJD2D is overexpressed in prostate tumors and promotes cancer cell growth.
  • Lysine methylation of JMJD2D at K427 by SET7/9 regulates its oncogenic function.
  • K427 mutation in JMJD2D impairs DU145 cell growth, invasion, and tumor formation.
  • JMJD2D activity influences the expression of CBLC (a ubiquitin ligase) and PLAGL1 (a transcription factor).
  • CBLC is upregulated in prostate tumors and its downregulation mimics the effects of the K427 mutation.

Conclusions:

  • A novel regulatory mechanism for JMJD2D via lysine methylation has been identified.
  • JMJD2D's pro-tumorigenic role in prostate cancer is mediated partly through regulation of CBLC expression.
  • CBLC exhibits a pro-tumorigenic role in prostate cancer, suggesting it as a potential therapeutic target.
  • JMJD2D and CBLC inhibitors may offer therapeutic benefits for prostate cancer treatment.
Keywords:
CBLCKDM4DPLAGL1gene expressionhistone demethylaseposttranslational modificationprostate cancer

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