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Journal of the American Academy of Dermatology
Volume 42, n° 5P1
pages 741-745 (mai 2000)
Doi : 10.1067/mjd.2000.103988
accepted : 26 October 1999
The expression of p16INK4a, the product of a tumor suppressor gene for melanoma, is upregulated in human melanocytes by UVB irradiation

Michael Piepkorn, MD, PhD
Division of Dermatology, Department of Medicine, and the Department of Pathology, University of Washington, Seattle. Seattle, Washington 


Background: The genetic locus CDKN2A has been linked to familial melanoma, and mutations or deletions in its coding sequence are seen in some cases of sporadic and familial melanomas. The protein encoded by CDKN2A, p16INK4a, functions as a negative regulator of cell cycle progression and as a tumor suppressor, but the regulatory mechanisms involved in controlling its expression remain poorly defined. Objective: This study tested the hypothesis that UVB irradiation, which transiently inhibits the growth of human melanocytes, is one of the regulators of p16INK4a expression. Methods: Cultured human melanocytes were irradiated with UVB over a sublethal dosage range, and p16INK4a protein and mRNA levels were quantified at varying times thereafter by quantitative immunostaining and by Western and Northern blotting. Results: Levels of p16INK4a protein in melanocytes increased significantly after sublethal UVB irradiation as compared with nonirradiated cells. Northern analysis indicated that p16INK4a messenger RNA coordinately increased in a dose-dependent manner more than 2-fold in irradiated cells at the tested doses. Conclusion: UVB irradiation transcriptionally activates the expression of p16INK4a in cultured human melanocytes. Therefore the growth arrest that occurs with irradiation of melanocytes could be mediated, in part, by upregulation of p16INK4a. This transient arrest may allow repair of UVB-induced DNA damage before cell division. Conversely, hereditary or acquired defects in CDK4A that give rise to functional insufficiency of p16INK4a could permit the premature propagation of melanocytes harboring potentially carcinogenic DNA damage. (J Am Acad Dermatol 2000;42:741-5.)

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 Supported in part by US Public Health Service grant AR 21557 from the National Institutes of Health, Department of Health and Human Services.
 Reprint requests: Michael Piepkorn, MD, PhD, Division of Dermatology, Box 356524, Seattle, WA 98195-6524.

© 2000  American Academy of Dermatology, Inc. Published by Elsevier Masson SAS@@#104157@@
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