REGULATION OF PHOSPHOLIPID TURNOVER IN HAMSTER FIBROBLASTS TRANSFORMED BY ONCOGENES V-SRC AND N-RAS

Phospholipid turnover was studied in two lines of golden hamster cells : in cells transformed by Rous sarcoma virus (line HET-SR) and in cell s additionally transfected with activated oncogene N-ras (line HET-SR- N-ras, clone 6). It was found that HET-SR cells are distinguished by a high level of phosphatidylcholine turnover and a relatively low level of phosphoinositide turnover. Transfection of the cells with activate d N-ras (HET-SR-N-ras line) inhibits phosphatidylcholine synthesis and activates phosphoinositide metabolism. Both cell lines retain sensiti vity to serum growth factors stimulating the rate of phospholipid turn over. In both cell lines dexamethasone reduces the rate of DNA synthes is and inhibits phosphatidylcholine and phosphoinositide turnover, Dex amethasone does not attenuate the predominant activation of phosphatid ylcholine synthesis in HET-SR cells or the activation of phosphoinosit ide synthesis characteristic for HET-SR-N-ras cells, The data suggest that the transduction of a mitogenic signal by growth factors in HET-S R and HET-SR-N-ras cells occurs via activation of phospholipid turnove r and is controlled by steroid hormones. The role of v-src and N-ras o ncogenes in transduction of mitogenic signal seems to be insignificant ; their activity is not controlled by dexamethasone.