Hepatitis B virus X protein (HBx) induces G2/M arrest and apoptosis through sustained activation of cyclin B1-CDK1 kinase

被引：50

作者：

Cheng, Ping

Li, Yuhua ^{[2
]}

Yang, Liping ^{[3
]}

Wen, Yanjun

Shi, Wei

Mao, Yongqiu

Chen, Ping

Lv, Huimin

Tang, Qingqing

Wei, Yuquan ^{[1
]}

机构：

[1] Sichuan Univ, W China Med Sch, W China Hosp, State Key Lab Biotherapy, Chengdu 610041, Peoples R China

[2] Sichuan Univ, Sch Life Sci, Chengdu 610041, Peoples R China

[3] Lanzhou Univ, Dept Med Oncol, Hosp 1, Lanzhou 730000, Gansu, Peoples R China

来源：

ONCOLOGY REPORTS | 2009年 / 22卷 / 05期

关键词：

HBV; HBx; hepatocellular carcinoma; G2/M arrest; apoptosis; vascular endothelial cells; CELL-CYCLE; HEPG2; CELLS; DNA-DAMAGE; CANCER; LIVER; GENE; P53; TRANSITION; CHECKPOINT; RETENTION;

D O I：

10.3892/or_00000542

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 ;

摘要：

Hepatitis B virus X protein (HBx) is a multifunctional 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.

引用

页码：1101 / 1107

页数：7

共 26 条

[1] HEPATITIS-B VIRUS HBX PROTEIN DEREGULATES CELL-CYCLE CHECKPOINT CONTROLS [J].