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Polycomb repressive complex 2 (PRC2) suppresses Eμ-myc lymphoma

Stanley C W Lee1, Belinda Phipson, Craig D Hyland

  • 1The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia; and.

Blood
|August 29, 2013
PubMed

Insights

Polycomb repressive complex 2 (PRC2) acts as a tumor suppressor in B-cell lymphoma. Loss of PRC2 function accelerates lymphomagenesis by enhancing B-lymphoid progenitor self-renewal, offering new insights into leukemia development.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • Polycomb group complexes, including PRC1 and PRC2, are crucial in regulating gene expression and are frequently deregulated in human cancers.
  • Mutations in PRC2-encoding genes (EZH2, EED, SUZ12) have varied roles in different leukemias, with inactivating mutations in some and gain-of-function mutations in others.

Purpose of the Study:

  • To investigate the specific role of PRC2 in Eµ-myc lymphomagenesis, a model for B-cell lymphoma.
  • To determine how alterations in PRC2 function impact B-lymphoid cell proliferation, apoptosis, cell cycling, and self-renewal.

Main Methods:

  • Utilized a mouse model of Eµ-myc lymphomagenesis.
  • Assessed the impact of heterozygosity for Suz12 or short hairpin RNA (shRNA)-mediated knockdown of Suz12 or Ezh2 on disease onset and progression.
  • Analyzed B-lymphoid cell accumulation, apoptosis, cell cycling, and serial clonogenicity of progenitor cells.

Main Results:

  • Loss of PRC2 function, through heterozygosity for Suz12 or knockdown of Suz12/Ezh2, significantly accelerated lymphomagenesis in the Eµ-myc model.
  • Accelerated disease onset was linked to increased accumulation of B-lymphoid cells, without significant changes in apoptosis or cell cycling.
  • Suz12-deficient B-lymphoid progenitors demonstrated enhanced serial clonogenicity, indicating increased self-renewal capacity.

Conclusions:

  • PRC2 functions as a tumor suppressor in the context of Eµ-myc lymphomagenesis.
  • Disruption of PRC2's normal function, specifically its role in restricting B-lymphoid progenitor self-renewal, contributes to lymphomagenesis.
  • These findings provide critical insights into the diverse roles of PRC2 mutations in various leukemias.

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