[Effect of specific activation of phosphatidylcholine metabolism in hamster fibroblasts transformed by Rous sarcoma virus].

Transformation of embryonic hamster fibroblasts by the Rous sarcoma virus results in sharp increase of the turnover rate of one of cellular phospholipids-phosphatidylcholine. The decrease in the rate of virus-transformed cells (HETSR strain) during the monolayer formation is attended by additional activation of phosphatidylcholine turnover. A similar effect is observed after prolonged culturing of cells with dexamethasone. Addition of the tyrosine kinase inhibitor, genistein, to cells leads to selective inhibition of phosphatidylcholine synthesis without any effect of phosphoinositide synthesis. Immunoblotting analysis of p60-src, the product of the viral oncogen v-src related to the tyrosine kinase family failed to produce any significant changes in protein synthesis and activity during dexamethasone-induced inhibition of HETSR cell growth. The data obtained testify to selective activation of phosphatidylcholine metabolism in src-transformed cells which enhances with a decrease in the rate of cell growth. The presence in HETSR cells of p60-src whose synthesis is not controlled by dexamethasone may be responsible for increased phosphatidylcholine metabolism and sustaining cell growth under conditions of limited activity of growth-promoting compounds.