Ehrlich ascites tumor cells produce a transforming growth factor-beta (TGFbeta)-like activity but lack receptors with TGFbeta-binding capacity.

Abstract

Ehrlich ascites tumor cells incorporate [methyl-3H]thymidine into DNA independently of exogenous growth factors or fetal calf serum. Using an acid/ethanol extraction procedure we have obtained from these tumor cells a fraction that induces both the proliferation and the formation of cell foci by Swiss 3T3 mouse fibroblasts in the presence of insulin; inhibits the proliferation of Mv1Lu mink lung epithelial cells; and stimulates the growth of NRK rat kidney fibroblasts in soft-agar in the presence of epidermal growth factor. An antibody against transforming growth factor-beta (TGFbeta) prevents both the tumor extract-induced proliferation of Swiss 3T3 fibroblasts and the tumor extract-induced proliferative arrest of Mv1Lu cells. The tumor cells secrete a TGF beta-like activity to the extracellular medium in a partially-activated form. However, authentic TGFbeta does not affect their proliferation, and no TGFbeta receptors were detected using [125I]TGFbeta as a ligand. Therefore, the absence of TGFbeta receptors with ligand-binding capacity in these tumor cells may bypass the negative control that this factor exerts on the proliferation of their normal cell counterparts.