Overexpression of DEK gene is correlated with poor prognosis in hepatocellular carcinoma.

Abstract

The oncogene DEK was originally identified as one of the parts of the DEK‑CAN fusion gene, arising from the translocation (6;9) in a subtype of acute myeloid leukemia. Since then, DEK has been shown to promote tumorigenesis in a variety of cancer cell types through its roles in inhibiting cell differentiation, senescence and apoptosis. Certain studies have established that DEK is dysregulated in several types of cancer, including hepatocellular carcinoma (HCC). However, its clinical significance in human HCC remains unknown. In this study, the expression of DEK mRNA and protein was examined in 55 surgical HCC specimens and matched non‑tumorous tissues. In addition, the correlation between DEK expression and clinicopathological characteristics and prognosis was analyzed. mRNA and protein levels of DEK were found to be significantly overexpressed in the majority of HCC tumors when compared with matched normal hepatic tissues (P<0.05). In addition, the expression pattern of DEK was closely correlated with differentiation status, portal venous invasion and tumor size (P<0.05). Kaplan‑Meier curves demonstrated that patients with higher DEK expression levels had significantly poorer survival than those with lower DEK expression levels (P=0.003). In addition, Cox regression analysis demonstrated that the level of DEK expression may be a valuable prognostic factor (P<0.05). These results suggested that DEK may play a significant role in hepatocyte differentiation and may serve as a useful prognostic marker and biomarker for the staging of HCC.