DMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin

Cited 3 time in scopus
Metadata Downloads
Title
DMBA/TPA-induced tumor formation is aggravated in human papillomavirus type 16 E6/E7 transgenic mouse skin
Author(s)
M O Kim; S H Kim; M J Shin; D H Yu; B S Kim; Kyu Tae Chang; S Lee; Y B Park; T H Lee; Z Y Ryoo
Bibliographic Citation
Oncology Research, vol. 16, no. 7, pp. 325-332
Publication Year
2007
Abstract
Human papillomavirus type 16 (HPV16) is a major causative factor in the development of uterine cervical carcinomas. We investigated the role of E6/E7 in tumor formation. Skin-specific E6/E7 transgenic mice showed approximately twice as many tumors compared with nontransgenic mice in dimethylbenz[a]anthracene (DMBA)-initiated and a 12-O-tetradecanoylphorbol-13-acetate (TPA)-promoted two-stage skin carcinogenesis. This model showed a significant increase of epidermal cell proliferation in the transgenic mice. The 8-hydroxy- 2'deoxyguanosine (8OH-dG) detection assay showed that oxidative DNA damage was significantly higher in the transgenic mice after TPA treatments. The overexpression of E6/E7 in the skin in the DMBA/TPA two-stage-induced carcinogenesis model aggravated the incidence of tumor formation. HPV16 E6/E7 appears to act as an enhancer of carcinogenesis that requires initiation by DMBA and promotion by TPA.
Keyword
DMBA/TPAhK14 promoterHPV16 E6/E7KeratinocytesSkin cancerTransgenic mice
ISSN
0965-0407
Publisher
Cognizant Communication Corp
DOI
http://dx.doi.org/10.3727/000000006783980964
Type
Article
Appears in Collections:
1. Journal Articles > Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.