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Redistribution of EZH2 promotes malignant phenotypes by rewiring developmental programmes.

Thomas Mortimer1, Elanor N Wainwright1, Harshil Patel2

  • 1Cancer Epigenetics Laboratory, The Francis Crick Institute, London, UK.

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|August 31, 2019
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Summary

Cancer cells hijack epigenetic regulators like EZH2, misusing developmental genes to promote tumor growth. Repressing EMX2 and de-repressing HOX genes drives glioma formation and sustains malignancy.

Keywords:
EZH2Polycombcancerchromatinglioblastoma

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Area of Science:

  • * Molecular biology
  • * Cancer research
  • * Epigenetics

Background:

  • * Epigenetic regulators are crucial for maintaining normal cell identity but are often co-opted by cancer cells.
  • * The Polycomb component Enhancer of Zeste Homolog 2 (EZH2) exhibits distinct roles in normal brain development and glioma, serving as a model to understand pathological functions of chromatin modifiers.
  • * Understanding how wild-type chromatin modifiers gain oncogenic functions is critical for developing targeted cancer therapies.

Purpose of the Study:

  • * To investigate how cancer cells repurpose key regulators of cell identity, specifically EZH2, to promote tumor development.
  • * To elucidate the mechanisms by which oncogenic signaling leads to the misregulation of developmental transcriptional programs in neural cells.
  • * To identify the specific gene expression changes associated with the acquisition and maintenance of tumorigenic potential in glioma.

Main Methods:

  • * Characterization of EZH2 targets in de novo transformed cells.
  • * Analysis of glioma patient datasets and cell lines.
  • * Functional studies involving forced expression of EMX2 in glioblastoma cells.

Main Results:

  • * Oncogenic signaling induces EZH2 redistribution across the genome, corrupting neural cell identity through misregulation of homeotic genes.
  • * Tumorigenic potential acquisition involves a transcriptional switch: de-repression of spinal cord-specifying HOX genes and silencing of forebrain neurogenesis regulator EMX2.
  • * EMX2 repression is essential for maintaining glioblastoma's tumorigenic potential, as forced EMX2 expression inhibits tumor formation.

Conclusions:

  • * Cancer cells subvert developmental transcriptional programs by redistributing EZH2, thereby corrupting normal cell identity.
  • * The repression of EMX2 and de-repression of HOX genes are critical events in glioma pathogenesis.
  • * Targeting EZH2-mediated epigenetic reprogramming offers a potential therapeutic strategy for brain tumors by restoring normal cell identity and proliferation control.