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Oncotarget

Overexpression of centromere protein K (CENP-K) gene in hepatocellular carcinoma promote cell proliferation by activating AKT/TP53 signal pathway.


PMID 29088763

Abstract

Hepatocellular carcinoma (HCC) is one of the high-incidence malignant tumors with very poor prognosis. Identification of potential oncogenes is critical to discovering novel therapeutic targets for many cancers, including HCC. In our previous studies, using microarray technology, we conformed that CENP-K was overexpressed in HCCs. However, whether the overexpression of CENP-K contributes to hepatocarcinogenesis remains unclear. In this study, we found that CENP-K was significantly up-regulated in 60% (63 of 105) of HCC specimens at the mRNA level compared to adjacent non-cancerous liver specimens, as determined by RT-qPCR. Immunohistochemical staining confirmed similar results at the protein level. Interestingly, we found that the DNA methylation status of the CENP-K promoter was significantly reduced in HCC specimens with increased CENP-K expression. In addition, CENP-K mRNA expression level was positively correlated with the level of alpha-fetoprotein (AFP) (≥ 400 ng/ml) and tumor size (≥ 3 cm) (