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EZH2 contributes to 5-FU resistance in gastric cancer by epigenetically suppressing FBXO32 expression

Chenyu Wang1, Xingwang Li1, Junjie Zhang1

  • 1Department of Anorectal, Huaihe Hospital of Henan University, Kaifeng, 475000, People's Republic of China, hujhhnuniver@126.com.

Oncotargets and Therapy
|November 23, 2018
PubMed
Abstract

Insights

Enhancer of zeste homologue 2 (EZH2) promotes gastric cancer chemoresistance by silencing FBXO32. EZH2 depletion overcomes 5-fluorouracil resistance, offering a new therapeutic target for gastric cancer.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • Enhancer of zeste homologue 2 (EZH2) is implicated in cancer chemoresistance.
  • Its specific role and mechanisms in gastric cancer (GC) chemoresistance remain unclear.

Purpose of the Study:

  • To investigate the role of EZH2 in 5-fluorouracil (5-FU) resistance in GC.
  • To elucidate the molecular mechanisms underlying EZH2-mediated chemoresistance.

Main Methods:

  • Analysis of EZH2 expression in 5-FU-resistant GC tissues and cell lines.
  • Assessment of EZH2 knockdown and FBXO32 overexpression effects on 5-FU sensitivity in GC cells.
  • In vivo studies to evaluate EZH2 inhibition in 5-FU-resistant GC models.

Main Results:

  • EZH2 was upregulated in 5-FU-resistant GC, correlating with poor prognosis.
  • EZH2 knockdown increased 5-FU sensitivity by epigenetically suppressing FBXO32.
  • FBXO32 overexpression mimicked EZH2 inhibition, while FBXO32 knockdown reversed it.
  • EZH2 inhibition enhanced 5-FU sensitivity in vivo.

Conclusions:

  • EZH2 depletion overcomes 5-FU resistance in GC by epigenetically silencing FBXO32.
  • EZH2 represents a potential therapeutic target for overcoming chemoresistance in gastric cancer.
Keywords:
5-FUFBXO32enhancer of zeste homologue 2gastric cancer

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