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Jmjd2c histone demethylase enhances the expression of Mdm2 oncogene

Akihiko Ishimura1, Minoru Terashima, Hiroshi Kimura

  • 1Division of Functional Genomics, Molecular & Cellular Targeting Translational Oncology Center, Cancer Research Institute, Kanazawa University, 13-1 Takara-machi, Kanazawa 920-0934, Japan.

Biochemical and Biophysical Research Communications
|September 8, 2009
PubMed

Insights

The Jumonji domain containing 2C (Jmjd2c) oncogene boosts Mdm2 expression by demethylating histone H3. This reduces the p53 tumor suppressor, promoting Jmjd2c-driven oncogenesis.

Area of Science:

  • Oncology
  • Epigenetics
  • Gene Regulation

Background:

  • Jmjd2c is a candidate oncogene encoding a histone lysine demethylase.
  • The role of Jmjd2c in regulating oncogenes like Mdm2 and tumor suppressors like p53 is under investigation.

Purpose of the Study:

  • To investigate the functional relationship between Jmjd2c and the Mdm2 oncogene.
  • To elucidate the mechanism by which Jmjd2c influences Mdm2 expression and p53 levels.

Main Methods:

  • Over-expression and siRNA-mediated knockdown of Jmjd2c.
  • Quantitative analysis of Mdm2 and p53 gene and protein expression.
  • Chromatin immunoprecipitation (ChIP) assay to assess Jmjd2c recruitment and histone modification at the Mdm2 promoter.

Main Results:

  • Jmjd2c over-expression increased Mdm2 oncogene expression in a demethylase-dependent manner.
  • Jmjd2c was recruited to the Mdm2 P2 promoter, causing demethylation of histone H3 lysine 9.
  • Knockdown of Jmjd2c reduced Mdm2 expression and consequently increased p53 levels.
  • These findings establish Mdm2 as a direct downstream target of Jmjd2c.

Conclusions:

  • Jmjd2c directly regulates Mdm2 oncogene expression through epigenetic modification of its promoter.
  • The Jmjd2c-Mdm2 axis, leading to p53 suppression, is a key mechanism in Jmjd2c-mediated oncogenesis.
  • Targeting Jmjd2c may offer a therapeutic strategy for cancers driven by this oncogene.

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