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Epigenetic Inactivation Implies a Tumor Suppressor Function in Hematologic Malignancies for Polo-Like Kinase 2 but not Polo-Like Kinase 3
Paul Smith, Nelofer Syed and Tim Crook
volume 5 | issue 12
15 june 2006Pages: 1262 - 1264
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The Polo-Like kinases (Plk) are a family of highly conserved cell cycle kinases, of which there are four members in humans. Whilst many studies support an oncogenic role for Plk1 in neoplasia, there is little definitive evidence at present to support involvement of the other family members in human cancer. Both Plk2 and Plk3 function in pathways of DNA damage response. Plk2 is a target gene for p53 and imposes a G2 checkpoint. More recent evidence reveals a novel function for Plk2 in mediating apoptosis in high-grade B lymphomas. Epigenetic inactivation of Plk2 via aberrant CpG methylation in the transcriptional regulatory elements of the gene is a common event in B cell neoplasia, whereas epigenetic inactivation of Plk3 is exceedingly rare in lymphomas. Further, in every case lacking Plk2 expression, there is concomitant over-expression of Plk3, consistent with functional degeneracy between the two proteins. These results imply that Plk2 may function as a tumour suppressor in hematologic neoplasia and have pharmaco-epigenomic implications.
We now provide open access to journal articles published online for one year or more. This article may be downloaded at the following link:
Download PDF If the document does not open, please right-click on the link (control-click on a Macintosh) and select the option to save the file to disk.