Overexpression of Polo-like kinase 1 (PLK1) in colorectal cancer (CRC) is independent of gene mutation and epigenetic alteration

![CDATA[Background. PLK1 is a serine/threonine kinase that promotes cell cycling and is involved in DNA damage response recovery. PLK1 overexpression is present in CRC, and it is associated with poor patient prognosis. However, the primary causes of its deregulation remain uncertain. Aims. This study investigated mutation and CpG island methylation of PLK1 in CRC and their associations with PLK1 overexpression. Methods. PLK1 gene in CRC cell lines was assessed by Sanger sequencing. The methylation status of CpG island of PLK1 promoter region were analysed by mass spectrometry. Subsequently the methylation study was expanded to a cohort CRC patients using pyrosequencing. Results. Sanger sequencing from the in vitro study detected single deletions in the silencer region (upstream of promoter region) of PLK1 gene in SW48 and a subpopulation of HCT116 cells. Secondly, irradiation did not trigger methylation in majority of the CG sites at CpG island of PLK1. In the patient cohort, low methylation of the CpG island of PLK1 was detected in CRC tissues and normal mucosa tissues and this was independent of PLK1 expression. Conclusions. In conclusion, overexpression of PLK1 does not appear to be related to intrinsic factors such as mutation or methylation may be the result of dysregulation of upstream proteins.]]