Plasma membrane and intracellular lipid synthesis in tumor cells rendered sensitive to humoral immune killing after treatment with metabolic inhibitors.
Line 10 guinea pigs hepatoma cells are resistant to killing by antibody and guinea pig complement. Metabolic inhibitors (adriamycin and actinomycin D) that increase the sensitivity of the cells to antibody-complement (C) killing were examined for their effects on the ability of the cells to synthesize and incorporate specific lipids into plasma membrane and intracellular membrane fractions. Drug-treated cells that had been rendered sensitive to antibody-C killing were inhibited in their incorporation of newly synthesized phosphatidylcholine and cholesteryl ester into the plasma membrane, as well as incorporation of phosphatidylcholine, cardiolipin, cholesteryl ester, and triglyceride into certain intracellular organelles including mitochondria, endoplasmic reticulum, nuclear membrane, or microsomes. Drug-treated cells recultured in the absence of the drug regained their ability to resist antibody-C killing and to synthesize and incorporate lipids into plasma and intracellular membranes. These data suggested that agents modifying the sensitivity of the tumor cells to humoral immune killing have a concomitant effect on plasma membrane and intracellular lipid synthesis.
D000818:Animals; D000920:Antibody-Dependent Cell Cytotoxicity / Q000187:drug effects*; D002462:Cell Membrane / Q000378:metabolism; D004317:Doxorubicin / Q000494:pharmacology*; D004351:Drug Resistance; D005472:Fluorouracil / Q000494:pharmacology*; D006168:Guinea Pigs; D008114:Liver Neoplasms, Experimental / Q000188:drug therapy* / Q000276:immunology / Q000378:metabolism; D008563:Membrane Lipids / Q000096:biosynthesis*
D008563:Membrane Lipids; D004317:Doxorubicin; D005472:Fluorouracil