E6 and E7 from beta HPV38 cooperate with ultraviolet light in the development of actinic keratosis-like lesions and squamous cell carcinoma in mice
- 1DKFZ, Heidelberg, Germany.
- 0DKFZ, Heidelberg, Germany.
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View abstract on PubMed
Summary
This summary is machine-generated.Beta human papillomavirus (HPV) oncoproteins E6 and E7 drive skin cancer development. Transgenic mice expressing these HPV38 proteins showed increased susceptibility to UV-induced squamous cell carcinoma (SCC).
Area Of Science
- Oncology
- Virology
- Dermatology
Background
- Cutaneous beta human papillomavirus (HPV) involvement in non-melanoma skin cancer (NMSC) is suspected but not fully established.
- Previous studies indicated transforming activities of HPV38 E6 and E7 oncoproteins.
Purpose Of The Study
- To assess the contribution of HPV38 to skin carcinogenesis using a novel transgenic mouse model.
- To investigate the role of HPV38 E6/E7 expression in epithelial proliferation and susceptibility to carcinogens.
Main Methods
- Generation of Keratin 14 (K14) promoter-driven transgenic mice expressing HPV38 E6 and E7 oncoproteins.
- Evaluation of epidermal proliferation, response to chemical carcinogenesis (DMBA/TPA), and UV irradiation exposure.
- Analysis of cell-cycle regulators (p21WAF1) and tumor development.
Main Results
- Transgenic mice exhibited increased epidermal proliferation compared to wild-type littermates.
- Mice were highly susceptible to chemical carcinogenesis and UV-induced skin lesions.
- UV irradiation led to reduced p21WAF1 accumulation and cell-cycle arrest in transgenic mice.
- Chronic UV exposure induced actinic keratosis-like lesions and squamous cell carcinoma (SCC) in transgenic mice, but not in wild-type controls.
Conclusions
- HPV38 E6 and E7 oncoproteins significantly contribute to skin SCC development.
- These oncoproteins enhance keratinocyte susceptibility to UV-induced carcinogenesis.
- The study provides a valuable model for investigating beta HPV-driven skin cancer.
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