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Integrin Distribution in Malignant Melanoma: Association of the ß₃ Subunit with Tumor Progression¹

Pulmonary Section, Department of Medicine, University of Pennsylvania [S. M. A., S. A. M.]; The Wistar Institute of Anatomy and Biology [S. M. A., S. A. M., L. D., M. H., C. A. B.]; Pigmented Lesion Study Group, Hospital of the University of Pennsylvania [D. E. E., R. S., M. H.]; and Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine [D. E. E.], Philadelphia, Pennsylvania 19104

Since tumor progression is dependent on the ability of malignant cells to interact with the extracellular matrix, molecules on the cell surface which mediate cell-substratum interactions are likely to be important regulators of tumor invasion and metastasis. The purpose of this study was to examine the distribution of one such group of cell adhesion receptors, the integrins, in benign and malignant lesions of human melanocytes. The distribution of integrin adhesion receptors was defined on cells in culture derived from normal and malignant melanocytes and in tissue sections from benign to increasingly malignant melanocytic lesions using a panel of monoclonal antibodies against specific integrin subunits. Cells in culture expressed a large variety of integrins, including all of the previously characterized members of the ß₁ subfamily plus the _v/ß₃ vitronectin receptor. The expression of integrins was similar in cells cultured from either benign or malignant lesions. In contrast, consistent differences were noted in integrin expression by cells within tissues containing metastatic and vertical growth phase melanomas when compared to radial growth phase melanoma cells and cells within nevi. Most notably, the expression of the ß₃ subunit was restricted exclusively to cells within vertical growth phase and metastatic melanomas. The presence of this integrin may be important in the development of tumor invasiveness and could be useful as a marker of melanoma cells entering the more aggressive phase of the malignant process.

¹ This work was supported by grants HL-01587 (S. A.) and HL 39023 (C. B.) from the National Heart, Lung and Blood Institute; grants CA-19144 (C. B.), CA10815, CA25294 (D. E.), and CA25874 (M. H.) from the National Cancer Institute; and grants from the W. W. Smith Charitable Trust and American Cancer Society (S. A.).

² To whom requests for reprints should be addressed, at 975 Maloney Building/H.U.P., 3600 Spruce Street, Philadelphia, PA 19104.

Received 4/17/90. Accepted 7/12/90.

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