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Cancer Cells Hijack PRC2 to Modify Multiple Cytokine Pathways

Mohamed Abou El Hassan1, Katherine Huang1, Manoja B K Eswara1

  • 1Lunenfeld Tanenbaum Research Institute, Mt Sinai Hospital, Toronto, Ontario, Canada.

Plos One
|June 2, 2015
PubMed

Insights

Polycomb Repressive Complex 2 (PRC2) epigenetically silences immune genes in cancer cells, distinct from non-cancer cells. Inhibiting PRC2 reactivates these immune pathways, offering new therapeutic strategies for cancer treatment.

Area of Science:

  • Epigenetics
  • Cancer Biology
  • Immunology

Background:

  • Polycomb Repressive Complex 2 (PRC2) is an epigenetic regulator implicated in tumorigenesis.
  • Cancers often evade immune detection through complex regulatory mechanisms.
  • The precise role of PRC2 in coordinating immune evasion in cancer remains unclear.

Purpose of the Study:

  • To investigate the role of PRC2 in regulating immune pathways within cancer cells.
  • To determine if PRC2's function in immune regulation is cancer-selective.
  • To explore the therapeutic potential of PRC2 inhibition on immune gene expression.

Main Methods:

  • RNA interference (RNAi) and EZH2 inhibitors were used to target PRC2.
  • Analysis of cytokine, cytokine receptor, and IFNγ stimulated gene (ISG) expression.
  • Chromatin immunoprecipitation (ChIP) to assess H3K27me3 and H3K4me3 marks.
  • Assessment of immune gene induction in the presence and absence of SWI/SNF.

Main Results:

  • PRC2 was found to repress hundreds of cytokine and ISG genes in a cancer-selective manner.
  • The repertoire of PRC2-repressed immune genes varied significantly across different cancer types.
  • PRC2 inhibition, via RNAi or EZH2 inhibitors, activated cytokine/cytokine receptor promoters.
  • PRC2 inhibition restored immune gene induction even in SWI/SNF-deficient cancers.

Conclusions:

  • PRC2 acts as a higher-order regulator of the immune program in cancer cells.
  • PRC2 inhibition enhances cancer cell responsiveness to immune signals.
  • This newly identified PRC2 function has significant implications for EZH2 inhibitor-based cancer therapies.

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