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Review Article: EZH2 in Pancreatic Cancer: Epigenetic Driver and Therapeutic Target

Talia Festekdjian1, Benjamin Bonavida2

  • 1Department of Microbiology, Immunology & Molecular Genetics, David Geffen School of Medicine, Jonsson Comprehensive Cancer Center, University of California at Los Angeles, Los Angeles, CA 90095, USA.

Critical Reviews in Oncogenesis
|February 9, 2026
PubMed

Insights

Pancreatic cancer (PDAC) is lethal due to high EZH2 expression, which drives resistance and immune evasion. New therapies targeting EZH2 are needed as current inhibitors are ineffective in PDAC.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal cancer with poor therapeutic response.
  • Overexpression of enhancer of zeste homolog 2 (EZH2) is implicated in PDAC pathogenesis, malignancy, and treatment resistance.
  • EZH2 contributes to immune evasion and an immunosuppressive tumor microenvironment, hindering immunotherapy efficacy.

Purpose of the Study:

  • To investigate the role of EZH2 in PDAC progression and therapeutic resistance.
  • To explore the potential of targeting EZH2 as a therapeutic strategy for PDAC.
  • To understand EZH2-mediated mechanisms contributing to treatment failure and immune evasion in PDAC.

Main Methods:

  • Analysis of EZH2 expression levels in PDAC patient cohorts.
  • Investigation of EZH2's role in gene regulation via polycomb repressive complex 2 (PRC2) activity.
  • Evaluation of EZH2's impact on tumor suppressor and apoptosis-related genes.
  • Assessment of EZH2's contribution to immune evasion and the tumor microenvironment.

Main Results:

  • High EZH2 expression in PDAC correlates with advanced stage, lymph node metastasis, and poor prognosis.
  • EZH2 promotes tumor aggressiveness by regulating cell cycle, proliferation, and differentiation genes.
  • EZH2-mediated epigenetic silencing contributes to resistance against conventional therapies and immune checkpoint inhibitors.
  • Current EZH2 inhibitors have shown limited clinical efficacy in PDAC.

Conclusions:

  • EZH2 is a critical driver of PDAC malignancy, therapeutic resistance, and immune evasion.
  • Targeting EZH2 presents a potential therapeutic avenue for PDAC, but novel strategies are required.
  • Further research into EZH2-mediated mechanisms is essential for developing effective PDAC treatments.

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