解析 HBx 突变体在肝癌缺氧环境中的多效作用。
Dissecting the pleiotropic actions of HBx mutants against hypoxia in hepatocellular carcinoma.
机构信息
1 Institute of Digestive Disease and Department of Medicine and Therapeutics, 2 State Key Laboratory of Digestive Disease, 3 School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong SAR, China ; 4 Shenzhen Research Institute, The Chinese University of Hong Kong, Shenzhen 518052, China.
出版信息
Hepatobiliary Surg Nutr. 2014 Apr;3(2):95-7. doi: 10.3978/j.issn.2304-3881.2014.02.07.
Error-prone integration of the hepatitis B virus X protein (HBx) into the hepatocellular genome generates a multitude of mutants exerting diverse effects on the development and progression of hepatocellular carcinoma (HCC). A recent study by Lai and colleagues revealed the disparate regulatory activity of clinically-predominant HBx mutants towards hypoxia-inducible factor-1α (HIF-1α), a central regulator of tumor angiogenesis, proliferation, metastasis and differentiation. These findings have shed insight into specific viral contribution of hypoxic response during hepatocarcinogenesis.
易错整合乙型肝炎病毒 X 蛋白（HBx）进入肝细胞基因组产生多种突变体，对肝细胞癌（HCC）的发展和进展产生多种影响。最近 Lai 及其同事的一项研究揭示了临床上主要的 HBx 突变体对缺氧诱导因子-1α（HIF-1α）的不同调节活性，HIF-1α 是肿瘤血管生成、增殖、转移和分化的中央调节剂。这些发现深入了解了肝癌发生过程中缺氧反应的特定病毒贡献。
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