DDX3, a DEAD box RNA helicase, is deregulated in hepatitis virus-associated hepatocellular carcinoma and is involved in cell growth control

摘要: Hepatocellular carcinoma (HCC) is one of the leading causes cancer deaths worldwide and highly correlated with hepatitis virus infection. Our previous report shows that a DEAD box RNA helicase, DDX3, targeted regulated by C (HCV) core protein, which implicates involvement DDX3 in HCV-related HCC development. In this study, potential role hepatocarcinogenesis investigated examining its expression surgically excised human specimens. Here we differential deregulation virus-associated HCC. A significant downregulation found HCCs from B (HBV)-positive patients, but not HCV-positive ones, compared to corresponding nontumor tissues. The differentially gender and, moreover, there tendency more frequent males than females. Genetic knockdown small interfering RNAs (siRNA) nontransformed mouse fibroblast cell line, NIH-3T3, results premature entry S phase an enhancement growth. This enhanced cycle progression linked upregulation cyclin D1 p21(WAF1) cells. addition, constitutive reduction increases resistance NIH-3T3 cells serum depletion-induced apoptosis enhances ras-induced anchorage-independent growth, indicating growth control. These findings together study suggest helicase growth-regulatory functions, involved HBV- HCV-associated pathogenesis.