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Background  Hepatocellular carcinoma (HCC), one of the most common cancers world-wide occurs twice as often in men compared to women. Predisposing conditions such as alcoholism, chronic viral hepatitis, aflatoxin B1 ingestion, and cirrhosis all contribute to the development of HCC.    Methods  We used a combination of methylation specific PCR and bisulfite sequencing, qReal-Time PCR (qPCR), and Western blot analysis to examine epigenetic changes for the  Polo-like kinases  ( Plks ) during the development of hepatocellular carcinoma (HCC) in  Plk4  heterozygous mice and murine embryonic fibroblasts (MEFs).    Results  Here we report that the promoter methylation of  Plk4  CpG islands increases with age, was more prevalent in males and that  Plk4  epigenetic modification and subsequent downregulation of expression was associated with the development of HCC in  Plk4  mutant mice. Interestingly, the opposite occurs with another Plk family member,  Plk1  which was typically hypermethylated in normal liver tissue but became hypomethylated and upregulated in liver tumours. Furthermore, upon alcohol exposure murine embryonic fibroblasts exhibited increased  Plk4  hypermethylation and downregulation along with increased centrosome numbers and multinucleation.    Conclusions  These results suggest that aberrant  Plk  methylation is correlated with the development of HCC in mice.

Aberrant methylation of Polo-like kinase CpG islands in Plk4 heterozygous mice