Ma. Krasilnikov et al., REGULATION OF PHOSPHOLIPID TURNOVER IN HAMSTER FIBROBLASTS TRANSFORMED BY ONCOGENES V-SRC AND N-RAS, Biochemistry, 59(11), 1994, pp. 1315-1320
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.