GFP/HPV-16E6 fusion protein induces apoptosis in MCF-7 and 293T cells using a transient expression system

被引:3
|
作者
Zhang, Ge
Liu, Yan [2 ]
Yu, Liwei [1 ]
Sun, Lina [3 ]
机构
[1] Beijing Haidian Hosp, Dept Gen Surg, Beijing 100080, Peoples R China
[2] Capital Med Univ, Beijing Obstet & Gynecol Hosp, Beijing 100026, Peoples R China
[3] Chinese Ctr Dis Control & Prevent, Natl Inst Infect Dis Control & Prevent, State Key Lab Infect Dis Prevent & Control, Beijing 102206, Peoples R China
关键词
human papillomavirus; high risk HPV-E6; green fluorescent protein; endogenous wild-type p53; apoptosis; PAPILLOMAVIRUS E6 PROTEIN; TUMOR-SUPPRESSOR PROTEIN; NUCLEAR-LOCALIZATION; HUMAN KERATINOCYTES; ONCOPROTEIN E6; P53; PROTEIN; DEGRADATION; STRESS; MDM2;
D O I
10.3892/or.2012.1976
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Since mucosal high-risk human papillomavirus (HPV) E6 can target and degrade the tumor suppressor p53, it is recognized as a major causative agent of cervical cancer. However, to date the distribution of high-risk HPV-E6 protein remains elusive. Thus, in the present study we used a mammalian green fluorescent protein (GFP) expression system to express a GFP/HPV-16E6 fusion protein (GFP-16E6) in wild-type (wt) p53 cells, such as MCF-7 and 293T cells to investigate the trafficking and localization of E6 and p53. Following transfection, we observed that the overexpressed GFP-16E6 was a nuclear protein, and that endogenous wt p53 localized to the nucleus together with GFP-16E6. Strikingly, p53 levels were not decreased but increased in 24 h transfected with pGFP-16E6. Furthermore, we observed significant apoptosis induced by GFP-16E6, which proved to be dependent on p53 expression.
引用
收藏
页码:1673 / 1680
页数:8
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