GROWTH-INHIBITION BY GLUCOCORTICOIDS IN RPMI-3460 MELANOMA-CELLS

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  • 1 January 1981
    • journal article
    • research article
    • Vol. 41  (8) , 3155-3160
Abstract
Dexamethasone inhibits the growth of RPMI 3460 melanoma [Syrian hamster] cells and cytosols of these cells contain a dexamethasone-binding macromolecule which has properties expected for a glucocorticoid receptor. Two other glucocorticoids, triamcinolone acetonide and hydrocortisone, also cause growth inhibition in RPMI 3460 cells; progesterone can block this response. The biological effect of these steroids correlates well with their previously reported ability to bind receptor, a result consistent with the concept that the glucocorticoid-induced growth inhibition is a receptor-mediated event. The nature of the growth response was investigated. Glucocorticoids inhibit growth in these melanoma cells by increasing the population-doubling time rather than by cytolytic effects. A limited exposure to dexamethasone fails to trigger the growth inhibition, suggesting that the continued presence of steroid is necessary for growth inhibition to occur. Since serum-free medium and medium conditioned by exposure to cells do not affect the glucocorticoid-induced growth inhibition, no evidence was obtained that either the interaction of glucocorticoids with serum factors or cell-induced changes in medium components are involved in the response. In addition to the effect on growth, morphological alterations were described which occur in the presence of dexamethasone.