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Originally published In Press as doi:10.1074/jbc.M212929200 on January 3, 2003

J. Biol. Chem., Vol. 278, Issue 11, 9790-9795, March 14, 2003
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Malignant Transformation of Melanocytes to Melanoma by Constitutive Activation of Mitogen-activated Protein Kinase Kinase (MAPKK) Signaling*

Baskaran GovindarajanDagger , Xianhe BaiDagger , Cynthia Cohen§, Hua Zhong, Susan Kilroy||, Gwendolyn Louis||, Marsha Moses||, and Jack L ArbiserDagger **

From the Departments of Dagger  Dermatology, § Pathology, and  Hematology/Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, Georgia 30322 and the || Department of Surgery, Children's Hospital, Harvard Medical School, Boston, Massachussetts 02115

Malignant melanoma is the cancer with the most rapid increase in incidence in the United States. Ultraviolet light and deficiency of the p16ink4a gene are known factors that predispose one to the development of malignant melanoma. The signal transduction pathways that underlie the progression of melanoma from their precursors, atypical nevi, are not well understood. We examined activation of the MAP kinase pathway in atypical nevi and melanoma cells and found that this pathway is activated in melanomas. To determine the functional significance of this activation, we introduced constitutively active MAP kinase kinase (MAPKK) into immortalized melanocytes. The introduction of this gene into melanocytes leads to tumorigenesis in nude mice, activation of the angiogenic switch, and increased production of the proangiogenic factor, vascular endothelial growth factor (VEGF), and matrix metalloproteinases (MMPs). Activation of MAP kinase signaling may be an important pathway involved in melanoma transformation. Inhibition of MAP kinase signaling may be useful in the prevention and treatment of melanoma.

* The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

** To whom correspondence should be addressed: Dept. of Dermatology, Emory University School of Medicine, WMB 5309, 1639 Pierce Dr., Atlanta, GA 30322. Tel.: 404-727-5063; Fax: 404-727-0923; E-mail: jarbise@emory.edu.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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