The Polo-like kinases as recipients and enablers of epigenetic modifications in tumourigenesis

TL;DRAbstract

Many highly conserved proteins have evolved specific niches in the cell cycle. For the Polo-like kinases (PLKs), these roles include centrosome duplication and maturation, the interaction with key DNA damage response proteins, cytokinesis, and chromosome separation. The PLKs deliver their effects via phosphorylation of their substrates at serine and threonine residues. Due to their importance in the cell cycle, expression of the PLKs is strictly governed. PLK deregulation is ubiquitously associated with malignancy. Elucidating how these proteins are regulated is key to understanding how their proper function can be restored in tumourigenesis. In recent years, the study of epigenetics as an additional mechanism controlling gene expression has come to the forefront. Epigenetic mechanisms include the addition or removal of methyl groups at the DNA and histone levels. My studies describe the regulation of PLK expression at the DNA level through the epigenetic mechanism of DNA methylation,

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