Protection against human papillomavirus type 16-E7 oncogene-induced tumorigenesis by in vivo expression of dominant-negative c-jun
✍ Scribed by Matthew R. Young; Linda Farrell; Paul Lambert; Parirokh Awasthi; Nancy H. Colburn
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 114 KB
- Volume
- 34
- Category
- Article
- ISSN
- 0899-1987
- DOI
- 10.1002/mc.10050
No coin nor oath required. For personal study only.
✦ Synopsis
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.