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DMBA/TPA-Induced Tumor Formation Is Aggravated in Human Papillomavirus Type 16 E6/E7 Transgenic Mouse Skin

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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.
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Keywords: DMBA/TPA; HPV16 E6/E7; Keratinocytes; Skin cancer; Transgenic mice; hK14 promoter

Document Type: Research Article

Affiliations: 1: School of Life Sciences and Biotechnology, College of Natural Sciences, Kyungpook National University, Daegu, 702-701, Korea 2: Laboratory of Primate Research, Korea Research Institute of Bioscience & Biotechnology, Oun-dong, Yusong-ku, Daejon 305-333, Korea 3: Department of Oral Biochemistry, School of Dentistry, Chonnam National University, 300 Yongbong-Dong, Buk-ku, Gwangju 500-757, Korea

Publication date: 2006-07-01

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