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A Potent Inhibitor of Normal and Transformed Cell Growth Derived from Contact-inhibited Cells¹

Department of Dermatology, New York University Medical Center, New York, New York 10016

Contact inhibition of growth (density-dependent regulation) is a form of in vitro growth control, the loss of which is correlated with in vivo tumorigenicity. A diffusible factor prepared from culture medium of a contact-inhibited line of hamster melanocytes has previously been found to restore the capacity for contact inhibition of growth to malignant melanocytes of man, mouse, and hamster, while also producing characteristic morphological changes. In the present studies the species specificity of the growth inhibitory effect was examined. The melanocyte contact inhibitory factor (MCIF) was found to inhibit growth in vitro of a broad spectrum of malignant cell types of ectodermal, mesodermal, and endodermal origin. Inhibition characterized by decreased saturation densities of cultures, growth in monolayers, and individual cell enlargement was dose dependent, reversible, and nontoxic at concentrations of <100 µg/ml. Neuroblastoma cells exhibited neurite differentiation. At higher concentrations (>100 to 200 µg/ml), MCIF was selectively lethal to malignant, non-contact-inhibited (compared to benign, contact-inhibited) cell types.

A fraction analogous to MCIF, prepared from culture medium of a line of contact-inhibited human epidermal cells and containing a protein electrophoretically identical with the major protein present in MCIF (M.W. about 160,000), was functionally identical with MCIF in both morphological and growth inhibitory effects on malignant melanocytes.

The growth regulatory macromolecular component(s) produced by contact-inhibited cells is able to restore some aspects of cell surface-mediated in vitro growth control to malignant cells. Such components may eventually provide a new class of cell surface-active agents for control of neoplastic growth.

¹ Supported by USPHS Grant CA 16013 from the National Cancer Institute, Department of Health, Education, and Welfare, by Grant CA 18034 from the National Cancer Institute through the National Large Bowel Cancer Project, by Postdoctoral Research Training Program Grant AM07190 from the National Institute of Arthritis and Metabolic Diseases, and by a donation from Michael Chernow through the Rudolf L. Baer Foundation for Skin Diseases, Inc.

² To whom requests for reprints should be addressed, at Department of Dermatology, School of Medicine, New York University Medical Center, 550 First Avenue, New York, N. Y. 10016.

Received 8/ 1/77. Accepted 12/ 8/77.

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