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KDM4B is a coactivator of c-Jun and involved in gastric carcinogenesis

Meng-Chen Wu1, Hsin-Hung Cheng1, Ta-Sen Yeh2

  • 1Institute of Molecular and Cellular Biology and Department of Life Science, National Tsing-Hua University, Hsinchu, 300, Taiwan.

Cell Death & Disease
|January 27, 2019
PubMed

Insights

KDM4B epigenetically upregulates Interleukin-8 (IL-8) in gastric cancer by interacting with c-Jun. This epigenetic regulation impacts H. pylori infection and suggests KDM4B as a therapeutic target for poor clinical outcomes.

Area of Science:

  • Epigenetics
  • Molecular Biology
  • Oncology

Background:

  • Jumonji C-containing histone lysine demethylases (KDM4A-D) are key epigenetic regulators.
  • Interleukin-8 (IL-8) is overexpressed in gastric cancer, but its epigenetic regulation is not fully understood.

Purpose of the Study:

  • To investigate the role of KDM4B in the epigenetic regulation of IL-8 in gastric cancer.
  • To explore the interaction between KDM4B, c-Jun, and IL-8 expression.

Main Methods:

  • Western blotting and quantitative PCR to assess gene and protein expression.
  • Chromatin immunoprecipitation assays to determine promoter interactions.
  • Cellular assays to evaluate cell migration and H. pylori interaction.

Main Results:

  • KDM4B, not KDM4A or KDM4C, upregulates IL-8 production in gastric cancer cells, with or without Helicobacter pylori.
  • KDM4B physically interacts with c-Jun at the IL-8, MMP1, and ITGAV promoters.
  • KDM4B depletion reduces integrin αV expression, hindering H. pylori-mediated IL-8 production and cell migration.
  • Elevated KDM4B expression correlates with increased p-c-Jun and poor clinical outcomes in gastric cancer patients.

Conclusions:

  • KDM4B is a critical regulator of JNK/c-Jun-driven processes in gastric cancer.
  • KDM4B represents a promising therapeutic target for gastric cancer treatment, particularly in cases associated with H. pylori infection.

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