A Role for Fatty Acid Composition of Complex Cellular Lipids in the Susceptibility of Tumor Cells to Humoral Immune Killing

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Abstract
Treatment of line-10 tumor cells with metabolic inhibitors (adriamycin, actinomycin D) or hormones (epinephrine, prednisolone) increases and decreases, respectively, the sensitivity of the cells to antibody-C mediated killing. Concomitantly, drug treatment inhibits the synthesis by the cells of specific complex lipids (cardiolipin, phosphatidyl choline, and triglycerides). Hormone treatment of these cells stimulates their synthesis of phosphatidyl choline and phosphatidyl serine and inhibits cardiolipin, phosphatidyl ethanolamine, and cholesteryl ester synthesis. Analysis of the newly synthesized fatty acids in the lipids extracted from drug-treated cells showed that the drug-induced sensitivity to antibody-C killing was accompanied by an increase in the amount of unsaturated fatty acids (C18:1, C18:2, and C18:3) in the cellular lipids. Cells washed free of drug and recultured in drug-free medium regained their resistance to antibody-C killing; these reverted cells had regained their ability to synthesize complex lipids and showed a fatty acid composition similar to that of untreated control cells. The effect of hormone treatment on the sensitivity of the cells to antibody-C killing could not be correlated with detectable changes in fatty acid synthesis. The results suggest that the drugs that increase the sensitivity of the cells to antibody-C killing may do so by altering the physical properties of the cell membrane through an effect on the synthesis of the fatty acid constituents of cellular lipids. Hormone treatment does not appear to affect the physical properties of the membrane by this mechanism.

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