Author/Authors :
lee, ying-ying chinese university of hong kong - state key laboratory of digestive disease, hong kong, china , lee, ying-ying chinese university of hong kong - institute of digestive disease - department of medicine and therapeutics, Shenzhen, China , mok, myth t.s. chinese university of hong kong - school of biomedical sciences, Hong Kong, China , mok, myth t.s. chinese university of hong kong - shenzhen research institute, shenzhen, china , cheng, alfred sze-lok chinese university of hong kong - shenzhen research institute, shenzhen, china , cheng, alfred sze-lok chinese university of hong kong - state key laboratory of digestive disease, Hong Kong, China , cheng, alfred sze-lok chinese university of hong kong - school of biomedical sciences, hong kong, china
Abstract :
Error-prone integration of the hepatitis B virus X protein (HBx) into the hepatocellulargenome generates a multitude of mutants exerting diverse effects on the development and progression ofhepatocellular carcinoma (HCC). A recent study by Lai and colleagues revealed the disparate regulatoryactivity of clinically-predominant HBx mutants towards hypoxia-inducible factor-1α (HIF-1α), a centralregulator of tumor angiogenesis, proliferation, metastasis and differentiation. These findings have shedinsight into specific viral contribution of hypoxic response during hepatocarcinogenesis.
Keywords :
Hepatitis B virus X protein mutant (HBx mutant) , hepatocellular carcinoma (HCC) , hypoxia , induciblefactor , 1α (HIF , 1α)
