[Regulation of the cycle of phospholipid turnover in hamster fibroblasts transformed by v-src and N-ras oncogenes].

The phospholipid turnover has been studied in two lines of golden hamster cells: in cells transformed by the Rous sarcoma virus (line HET-SR) and in cells additionally transfected with the activated oncogene N-ras (line HET-SR-N-ras, clone 6). It has been found that HET-SR cells are distinguished by a high level of phosphatidylcholine turnover and a relatively low level of phosphoinositide turnover. Transfection of cells with the activated N-ras (line HET-SR-N-ras) leads to the inhibition of phosphatidylcholine synthesis and activation of phosphoinositide metabolism. Both cell lines preserve their sensitivity to serum growth factors stimulating the rate of phospholipid turnover. In both cell lines dexamethasone decreases the rate of DNA synthesis and inhibits the phosphatidylcholine and phosphoinositide turnover. At the same time, dexamethasone does not influence the predominant activation of phosphatidylcholine synthesis in HET-SR cells or the activation of phosphoinositide synthesis characteristic of HET-SR-N-ras cells. The data obtained suggest that the transmission of the mitogenic signal from growth factor in HET-SR and HET-SR-N-ras cells occurs via the activation of the phospholipid turnover and is controlled by steroid hormones. The role of v-src and N-ras oncogens in the transmission of the mitogenic signal seems to be insignificant; their activity is not controlled by dexamethasone.