Insulin promotes the growth of F9 embryonal carcinoma cells apparently by acting through its own receptor

Abstract

Low concentrations of insulin (20 to 40 ng/ml) stimulate the growth of F9 embryonal carcinoma cells under defined, serum-free conditions. [ 125I] Insulin binding studies reveal the presence of high and low affinity receptor sites, and insulin does not compete for [ 125I] multiplication-stimulating activity (MSA) binding to F9 cells. The addition of antibodies to the insulin receptor (anti R) to serum-free growth medium also promotes F9 cell proliferation. Anti R blocks [ 125I] insulin binding to F9 cells, but does not alter the binding of [ 125I] MSA, indicating that anti R is exerting its growth-promoting effects by interacting with the insulin receptor. These results demonstrate that F9 cells do possess specific insulin receptors and establish that insulin stimulates the growth of these cells by acting directly through its own receptor and not through the MSA receptor also present on these cells.