[3H] hexadecanoic and N-acetyl [14C]
neuraminic acids were incorporated in glycerolipids or
gangliosides of 2 rat colon
carcinoma cell lines, having (PRO cells), or not (REG cells) invasive capacities when inoculated in syngeneic BD IX rats. The cells were cultured (48 h) in presence of 1-0-octadecyl-2-0-methyl-3-phosphocholine (ET 18-0-CH3) 20 or 40 microM, which, on transformed cells, inhibits the cell growth, modifies the glycerolipid biosynthesis, and activates the
sialyltransferases. ET 18-0-CH3 20 microM activated, in PRO and in REG cells the incorporation of [3H] hexadecanoate in
monosialogangliosides (1.45 fold compared to controls), but not in
disialogangliosides and the distribution of this
fatty acid between monosialo- (82%) and
disialogangliosides (18%) was unchanged with controls. After [14C] neuraminic
acid labelings, and for control experiments, the total radioactivities in
gangliosides, in PRO cells, were twice higher than in REG cells, a difference which, probably, reflects the
ganglioside content. ET 18-0-CH3 20 microM did not increase the incorporation of the [14C] neuraminic
acid in PRO and in REG cells, and did not change its distribution between monosialo (70-80% for controls and experiments with ET 18-0-CH3) and
disialogangliosides (20-30%). Similar results were obtained with ET 18-0-CH3 40 microM for the distribution of [14C] neuraminic
acid in monosialo- and
disialogangliosides. Whatever the precursor, the trisialogangliosides were never radiolabeled. Analysis of the [3H] glycerolipids (the main radiolabeled
lipid classes in controls were:
phosphatidylcholines,
triglycerides,
sphingomyelins and phosphatidyl-inositols) revealed that ET 18-0-CH3, compared to controls, did not activate the incorporation of [3H] hexadecanoate in total glycerolipids (PRO or REG cells). It activated (3 fold) its incorporation in triglyerides, inhibited it (0.5-0.6 fold) in
phosphatidylcholines,
sphingomyelins and phosphatidyl-inoditols and all these most noticeable differences were observed in PRO and in REG cells. These findings reflect the impossibility of ET 18-0-CH3 to activate the
sialyltransferases during the
ganglioside biosynthesis in colon
carcinoma cells, while it modified
ceramide,
glycerophospholipid and neutral glycerolipid biosynthesis.