期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 165, 期 3, 页码 879-887出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0002-9440(10)63350-0
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资金
- NCI NIH HHS [CA 088943, CA 16672, R01 CA046523, CA 46523, P30 CA016672, R01 CA088943] Funding Source: Medline
- NIEHS NIH HHS [ES07784, P30 ES007784] Funding Source: Medline
inhibition of P53-induced epidermal apoptosis, generation of p53 mutations, and suppressor T cells are the critical events responsible for the induction and development of UV-induced skin cancers. Recently, we demonstrated that CD1d knockout mice were resistant to UV-induced immunosuppression, prompting us to further address the role of CD1d in regulating LTV carcinogenesis. We, therefore, investigated the response of wild-type (WT) and CD1d-/- mice to UV carcinogenesis. We found that although 100% of WT mice developed skin tumors after 45 weeks of UV irradiation, only 60% of CD1d-/- mice developed skin tumors. Surprisingly, keratinocytes and fibroblasts from CD1d-/- mice were more sensitive to UV-induced apoptosis and persisted longer than cells derived from WT mice. In addition, epidermis and dermis taken from chronically UV-irradiated CD1d-/- mice harbored significantly fewer p53 mutations than WT mice. our findings identify an unexpected and novel function for CD1d as a critical molecule regulating UV carcinogenesis, by inhibiting apoptosis to prevent elimination of potentially malignant keratinocytes and fibroblasts.
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