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In Vitro Growth Inhibition of Human Malignant Melanoma Cells by Glucocorticoids

Oncology Research Laboratory, Nassau Hospital, Mineola, New York 11501 [D. M. D., B. M., L. N.], and State University of New York, School of Medicine, Stony Brook, New York 11790 [L. N.]

The human malignant melanoma cell line, NEL, was found to contain glucocorticoid receptors. When the binding data were analyzed according to the method of Scatchard, results indicated a ligand binding capacity of 247 fmol/mg protein and a K_d of 1 x 10^-9 M. Additional studies show that the continuous incubation of NEL cells with triamcinolone acetonide (TA) for 72 hr results in a 30% inhibition in cell growth. To ascertain the mechanism by which glucocorticoids inhibit the growth of NEL cells, uptake and incorporation studies were carried out using various ³H precursors. Results indicate that, after 4 hr of TA treatment, a modest inhibition in [³H]thymidine uptake was observed, while stimulation of [³H]thymidine incorporation was noted at all steroid concentrations tested. However, cells incubated for 18 hr with TA (concentration, 10^-8 M) showed a 30% decrease in the amount of [³H]thymidine incorporated into DNA. TA had no effect on [³H]leucine or [³H]glucose uptake after 4 hr of treatment but did inhibit [³H]glucose (42%) uptake after 18 hr of treatment. A slight stimulation (9%) in [³H]leucine incorporation was observed at this time point. When NEL cells were incubated with TA and the antiglucocorticoid, progesterone, the inhibition in [³H]thymidine incorporation was negated. These findings indicate that glucocorticoids exert some influence on the growth of human melanoma cells, and this effect is mediated through the glucocorticoid receptor.

¹ To whom requests for reprints should be addressed, at Oncology Research Laboratory, Nassau Hospital, 259 First Street, Mineola, N. Y. 11501.

Received 12/13/82. Accepted 3/11/83.

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