Abstract
PG19 mouse melanoma cells arrest growth when they become confluent in medium containing low concentrations of serum. Under these conditions, insulin does not stimulate DNA synthesis in the mouse melanoma cells, whereas it does in mouse embryo fibroblats and fibroblast × melanoma hybrids. A detailed examination of the binding of insulin to the melanoma cells and fibroblast × melanoma hybrids in the presence of bacitracin has shown that they have approximately equal numbers of insulin receptors, and that these receptors have similar affinities for insulin. These results indicate that the unresponsiveness of the melanoma cells to the mitogenic action of insulin is not attributable to a lack of insulin receptors. Although insulin does not stimulate incorporation of ^3^Hthymidine into DNA in confluent cultures of the melanoma cells, it does stimulate uptake of α‐aminoisobutyrate, indicating that the insulin receptors are functional and that insulin elicits an acute response in these cells. In hormone‐supplemented serum‐free medium, insulin does not stimulate growth of the melanoma cells, while it does stimulate growth of the fibroblast × melanoma hybrid. This suggests that an acute response to insulin is not sufficient for stimulation of growth either in confluent growth‐arrested cells or in exponentially growing cells in serum‐free medium.