Cheng Ping, Li Yuhua, Yang Liping, Wen Yanjun, Shi Wei, Mao Yongqiu, Chen Ping, Lv Huimin, Tang Qingqing, Wei Yuquan
State Key Laboratory of Biotherapy, West China Hospital, School of Life Science, Sichuan University, Sichuan 610041, PR China.
Oncol Rep. 2009 Nov;22(5):1101-7. doi: 10.3892/or_00000542.
Hepatitis B virus X protein (HBx) is a multi-functional regulatory protein that is known to be involved in viral proliferation, transcriptional activation and cell growth control. However, the actual role of HBx in cell growth control remains controversial. In this study, the impact of HBx on cell growth in vitro and in vivo was further investigated. HBx was able to inhibit the growth of hepatocellular carcinoma (HCC) cells and induce G2/M arrest in vitro. Moreover, unlike many other G2/M arrest mechanisms, HBx did not inhibit cyclin B1-CDK1 kinase activity, but it persistently activated the cyclin B1-CDK1 kinase. In vivo, HBx inhibited tumor cell growth and induced apoptosis as well as inhibited the growth of vascular endothelial cells. In conclusion, HBx induced G2/M arrest and apoptosis through sustained activation of cyclin B1-CDK1 kinase, and negatively regulated cell growth in vitro and in vivo.
乙型肝炎病毒X蛋白（HBx）是一种多功能调节蛋白，已知其参与病毒增殖、转录激活和细胞生长控制。然而，HBx在细胞生长控制中的实际作用仍存在争议。在本研究中，进一步研究了HBx对体外和体内细胞生长的影响。HBx能够在体外抑制肝癌（HCC）细胞的生长并诱导G2/M期阻滞。此外，与许多其他G2/M期阻滞机制不同，HBx并不抑制细胞周期蛋白B1-CDK1激酶活性，而是持续激活细胞周期蛋白B1-CDK1激酶。在体内，HBx抑制肿瘤细胞生长并诱导凋亡，同时抑制血管内皮细胞的生长。总之，HBx通过持续激活细胞周期蛋白B1-CDK1激酶诱导G2/M期阻滞和凋亡，并在体外和体内对细胞生长起负调控作用。
