CtIP function plays a role in hepatitis B related hepatocellular carcinoma

Researchers have proposed a new molecular pathway underlying the occurrence of hepatitis B related hepatocellular carcinoma.

Hepatitis B is a potentially life-threatening liver infection caused by the hepatitis B virus (HBV). It is a major global health problem. It can cause chronic infection and puts people at high risk of death from cirrhosis and hepatocellular carcinoma (HCC). 

HCC is the sixth most common and aggressive malignancies, and ranks as the third leading cause of cancer-related death all over the world. Over the past 20 years, the mortality rate resulted from HCC has rose significantly. Dysregulation of DNA double-strand break (DSB) repair may explain the pathogenesis of HBV-related HCC. 

Hepatocellular DSB could lead to HCC development, while evidences have shown that HBV induces DSB while hinders DSB repair in host hepatocytes. Tumour suppressor protein CtIP plays a critical role in DSB repair. Whether HBV could affect CtIP expression of hepatoma cell remains unclear.

A study led by Dr. Dongxin Zhang at the Huazhong University of Science and Technology investigated whether HBV affects CtIP expression in DSB repair of hepatoma cell. Researchers found that the change of CtIP expression and phosphorylation in DSB of hepatoma cells upon HBV infection provides strong experimental support for their hypothesis that CtIP is dysregulated by HBV in hepatocyte DSB. Relying on the results gathered by using bleomycin-induced DSB model and HBV-infective hepatoma cell model, this study provides further evidence that HBV-mediated abnormality in CtIP function may be a potential causal factor for the pathogenesis of HCC.

The findings from this study suggest a molecular pathway underlying the occurrence of HCC, providing new insights into the pathophysiology of HCC.

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