The human papillomavirus-16 (HPV-16) oncoprotein E7 conjugates with and mediates the role of the transforming growth factor-beta inducible early gene 1 (TIEG1) in apoptosis

被引：10

作者：

Chang, Hung-Shu ^{[1
]}

Lin, Ching-Hui ^{[2
]}

Yang, Chien-Hui ^{[2
]}

Liang, Yuh-Jin ^{[2
]}

Yu, Winston C. Y. ^{[2
]}

机构：

[1] Natl Cheng Kung Univ, Coll Biosci & Biotechnol, Dept Life Sci, Tainan 70101, Taiwan

[2] Natl Hlth Res Inst, Natl Inst Canc Res, Miaoli Cty, Taiwan

来源：

INTERNATIONAL JOURNAL OF BIOCHEMISTRY & CELL BIOLOGY | 2010年 / 42卷 / 11期

关键词：

HPV; E7; TIEG1; Apoptosis; Cervical cancer; RISK HUMAN PAPILLOMAVIRUSES; TGF-BETA; TUMOR-SUPPRESSOR; PROTEINS; CANCER; INHIBIT; CELLS; E6;

D O I：

10.1016/j.biocel.2010.07.019

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The human papillomavirus (HPV) oncoprotein E7 is a major transforming protein. The E7 protein does not possess intrinsic enzymatic activity, but rather functions through direct and indirect interactions with cellular proteins, several of which are well known cellular tumor suppressors. Using the yeast two-hybrid system, we found that transforming growth factor-beta inducible early gene 1 (TIEG1), a member of the Kruppel-like family (KLF) that has been implicated as a putative tumor suppressor, interacts and forms a specific complex with HPV-16 E7. TIEG1 has been shown to mimic the effects of TGF-beta in various carcinoma cells and plays a critical role in the apoptotic cascade. Our results indicate that E7 binds to the C-terminus of TIEG1 and induces its degradation via the ubiquitin pathway. E7 not only increased the ubiquitination of TIEG1 but also influenced the ability of TIEG1 to affect apoptosis. Our results suggest that suppression of TIEG1-mediated signaling by E7 may contribute to HPV-associated carcinogenesis. (C) 2010 Elsevier Ltd. All rights reserved.

引用

页码：1831 / 1839

页数：9