Primary liver cancer is the fifth most common cancer worldwide and the third most common cause of cancer mortality, and hepatocellular carcinoma (HCC) accounts for between 85% and 90% of primary liver cancers. Keywords: CtIP, double-strand break, hepatitis B virus, hepatocellular carcinoma, phosphorylation. These results suggest that HBV could interfere CtIP via enhancing its expression while dampening its phosphorylation, which may disrupt DSB repair pathways and implicate CtIP dysfunction in HBV-related HCC. However, p-CtIP of HepG2.2.15 was significantly lower than that of HepG2 after DSB. Phosphorylated CtIP (p-CtIP, serine site) was even lower than detectable limit in both HepG2 and HepG2.2.15 before DSB. CtIP protein expression was the same pattern as its gene expression. CtIP gene expression was significantly upregulated after DSB in both HepG2 and HepG2.2.15, while CtIP expression of HepG2.2.15 was higher than that observed in HepG2 before and after DSB. Bleomycin treatment could result in DSB by γ-H2AX detection. The two cell lines were treated with bleomycin to induce DSB. HepG2.2.15 was selected as the HBV positive hepatoma cell line, while HepG2 as the HBV negative hepatoma cell line. The purpose of present study was to clarify whether HBV affects CtIP expression in DSB repair of hepatoma cell. Tumor suppressor CtIP plays a critical role in DSB repair.
Dysregulation of DNA double-strand break (DSB) repair may explain the pathogenesis of HBV-related HCC. Hepatitis B virus (HBV) infection is a leading cause for hepatocellular carcinoma (HCC). Select the file that you have just downloaded and select import option Reference Manager (RIS).
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