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Protection against human papillomavirus type 16‐E7 oncogene‐induced tumorigenesis by in vivo expression of dominant‐negative c‐ jun †
Author(s) -
Young Matthew R.,
Farrell Linda,
Lambert Paul,
Awasthi Parirokh,
Colburn Nancy H.
Publication year - 2002
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/mc.10050
Subject(s) - biology , carcinogenesis , oncogene , human papillomavirus , in vivo , oncogene proteins , cancer research , virology , genetics , microbiology and biotechnology , gene , regulation of gene expression , medicine , cell cycle
Expression of the human papillomavirus (HPV) type 16 E6 and E7 gene products is a risk factor for human cervical carcinogenesis as well as skin and oral carcinogenesis. Expression of the HPV‐16 E7 gene in mouse skin induces hyperplasia and enhances tumor promotion. Expression of dominant‐negative c‐ jun (TAM67) in the mouse skin protects mice from 7,12‐dimethylbenz[ a ]anthracene (DMBA)/12‐ O ‐tetradecanoylphorbol‐13‐acetate (TPA)–induced papillomagenesis without blocking mitogen‐induced hyperproliferation. To determine the role of activator protein‐1 (AP‐1) in HPV‐induced cancer, we crossed HPV‐16 E7 mice with TAM67 mice and analyzed the effects of DMBA/TPA on tumor promotion. We showed that expression of TAM67 protected mice from HPV‐16 E7–enhanced tumorigenesis, suggesting AP‐1 as a target for prevention of HPV‐induced cancer. Published 2002 Wiley‐Liss, Inc.