Mechanism of D-bifunctional Protein Promoting Formation of Hepatocellular Carcinoma in Rat via STAT3

Abstract

Objective To investigate the expression of D-bifunctional protein (DBP) in hepatocarcinoma tissues of rat and its correlation with signal transducer and activator of transcription 3(STAT3). Methods Rat model of hepatocellular carcinoma(HCC) was induced by intraperitoneal injection of diethylnitrosamine(DEN). HE staining and serum biochemical indicators were used to detect liver pathological severity in HCC rats. Western blot, immunohistochemistry and qRT-PCR were used to detect the expression of DBP, PCNA, cyclinD1, p-STAT3, p-Akt, p-MEK and p-ERK. Results DEN induced severe liver deterioration in HCC rats. The expression of DBP in liver tissues of HCC rats was higher than that in normal rat liver. The mRNA expression of PCNA and cyclin D1 in HCC group were significantly higher than those in normal control(NC) group, and the expression of DBP was positively correlated with PCNA and cyclin D1 expression. The over-expression and knockdown of DBP increased and decreased the number of cells and the expression of PCNA, cyclin D1 protein in HepG2 cells, respectively. The expression of p-STAT3 was significantly increased in HCC group, and positively correlated with DBP expression. The protein levels of p-Akt, p-MEK and p-ERK were also significantly enhanced compared with the NC group. Conclusion Highly-expressed DBP plays a catalytic role in the development of rat liver cancer.

Keywords

• dbp
• stat3
• hepatocellular carcinoma
• cyclind1
• pcna