Ma. Krasilnikov et al., SPECIFIC ACTIVATION OF PHOSPHATIDYLCHOLINE TURNOVER IN HAMSTER FIBROBLASTS TRANSFORMED BY THE ROUS-SARCOMA VIRUS, Biochemistry, 61(3), 1996, pp. 388-392
Transformation of hamster embryonic fibroblasts by the Rous sarcoma vi
rus caused a sharp increase in the turnover of phosphatidylcholine, a
cellular phospholipid. A decrease in the growth rate of the Rous-sarco
ma-virus-transformed cells (HETSR strain) is accompanied by an additio
nal activation of phosphatidylcholine metabolism during monolayer form
ation. A similar effect is observed after prolonged culturing of the c
ells in the presence of dexamethasone. Addition of the tyrosine kinase
inhibitor genistein selectively inhibits phosphatidylcholine synthesi
s without affecting the synthesis of phosphoinositides. Immunoblotting
analysis of the p60-src protein (a product of the v-src viral oncogen
e of the tyrosine kinase family) failed to reveal significant changes
in the synthesis and activity of this protein during the dexamethasone
-induced inhibition of HETSR cell growth. These results suggest select
ive activation of phosphatidylcholine metabolism in the src-transforme
d cells increasing with the decrease in the cell growth rate. The p60-
src synthesis does not depend on dexamethasone, and its presence in th
e HETSR cells is suggested to be one of the factors responsible for th
e increased level of phosphatidylcholine metabolism, thereby promoting
cell growth under the limited activity of growth substances.