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Dispensability of p53 degradation for tumorigenicity and decreased serum requirement of human papillomavirus type 16 E6
Author(s) -
Inoue Tadao,
Oka Kiyomasa,
YongII Hwang,
Vousden Karen H.,
Kyo Satoru,
Jing Pan,
Hakura Akira,
Yutsudo Masuo
Publication year - 1998
Publication title -
molecular carcinogenesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.254
H-Index - 97
eISSN - 1098-2744
pISSN - 0899-1987
DOI - 10.1002/(sici)1098-2744(199803)21:3<215::aid-mc9>3.0.co;2-k
Subject(s) - biology , transactivation , carcinogenesis , mutant , gene , human papillomavirus , cancer research , transformation (genetics) , mutation , wild type , cell growth , microbiology and biotechnology , virology , gene expression , genetics , medicine
Certain types of human papillomavirus (HPV), such as types 16 and 18, are etiological agents for carcinogenesis of the uterine cervix. These HPVs have two oncogenes, E6 and E7 , that have transforming activities in established murine cells. Tumorigenicity and decreased serum requirement for cell growth are conferred by the E6 gene, whereas anchorage‐independent growth is mainly governed by the E7 gene. To understand the mechanism of cellular transformation by the HPV16 E6 gene, we examined three mutant E6 proteins defective for p53 binding, p53 degradation, or transactivation of the adenovirus E2 promoter for the ability to induce tumorigenicity and decreased serum requirement. The results showed that tumorigenicity and decreased serum requirement were associated with the ability of E6 to bind to p53, although the subsequent degradation of p53 was not required for these functions. Mol. Carcinog. 21:215–222, 1998. © 1998 Wiley‐Liss, Inc.