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Epigenetic inactivation implies a tumor suppressor function in hematologic malignancies for Polo-like kinase 2 but

Paul Smith1, Nelofer Syed, Tim Crook

  • 1Cancer Genetics and Epigenetics Laboratory, The Toby Robins Breakthrough Breast Cancer Centre, Institute for Cancer Research, London, England.

Cell Cycle (Georgetown, Tex.)
|July 27, 2006
PubMed

Insights

Polo-Like Kinase 2 (Plk2) may act as a tumor suppressor in blood cancers. Aberrant methylation often silences Plk2, leading to Plk3 overexpression, suggesting a link between Plk2 inactivation and lymphoma development.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Epigenetics

Background:

  • Polo-Like Kinases (Plk) are conserved cell cycle regulators.
  • Plk1 is implicated in cancer, but roles of other Plks are less clear.
  • Plk2 and Plk3 are involved in DNA damage response pathways.

Purpose of the Study:

  • Investigate the role of Plk2 and Plk3 in hematologic neoplasia.
  • Examine epigenetic regulation of Plk2 and Plk3 in B cell lymphomas.
  • Determine functional relationships between Plk2 and Plk3.

Main Methods:

  • Analysis of Plk2 and Plk3 expression in B cell lymphomas.
  • Assessment of CpG methylation in Plk2 and Plk3 regulatory regions.
  • Correlation of gene expression with methylation status.

Main Results:

  • Plk2 inactivation via CpG methylation is common in B cell neoplasia.
  • Plk3 is frequently overexpressed when Plk2 is epigenetically silenced.
  • Epigenetic inactivation of Plk3 is rare in lymphomas.

Conclusions:

  • Plk2 likely functions as a tumor suppressor in hematologic cancers.
  • Aberrant methylation of Plk2 has implications for B cell neoplasia.
  • Functional redundancy between Plk2 and Plk3 suggests pharmaco-epigenomic strategies.

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