Duksin D, Bornstein P
Proc Natl Acad Sci U S A. 1977 Aug;74(8):3433-7. doi: 10.1073/pnas.74.8.3433.
Normal and virally transformed mouse (3T3) and human (WI-38) cells were treated with tunicamycin, an inhibitor of lipid-carrier-dependent glycosylation of proteins. Incubation of cells with tunicamycin (1 microgram/ml) caused detachment and death of simian virus 40- and polyoma-transformed cells within 24 hr; these effects were not seen with nontransformed cell lines. However, the proliferation of 3T3 cells was inhibited by tunicamycin and, after a few days, a distinct change from an epithelioid to an abnormally elongated shape was observed. Both inhibition of growth and the morphological changes were reversible. A marked decrease in concanavalin A agglutinability was observed in virally transformed cells treated with tunicamycin (0.5 microgram/ml), but agglutination by wheat germ agglutinin or soybean agglutinin was unaffected. Analysis of biosynthetically labeled proteins showed that a high-molecular-weight protein, presumed to be related to fibronectin, is markedly reduced in the medium of cells cultured in the presence of tunicamycin. These results suggest that tunicamycin interferes with the insertion or function of one or more cell-surface glycoproteins. Such cell-surface changes could affect a number of cellular properties, including attachment, cell shape, and agglutinability by some lectins.
用衣霉素（一种蛋白质脂质载体依赖性糖基化的抑制剂）处理正常的以及经病毒转化的小鼠（3T3）和人（WI - 38）细胞。用衣霉素（1微克/毫升）孵育细胞，会导致猿猴病毒40和多瘤病毒转化的细胞在24小时内发生脱离和死亡；这些效应在未转化的细胞系中未观察到。然而，衣霉素会抑制3T3细胞的增殖，并且在几天后，可以观察到细胞从上皮样形态明显转变为异常伸长的形态。生长抑制和形态变化都是可逆的。在用衣霉素（0.5微克/毫升）处理的病毒转化细胞中，观察到伴刀豆球蛋白A凝集性显著降低，但小麦胚凝集素或大豆凝集素的凝集不受影响。对生物合成标记蛋白质的分析表明，在衣霉素存在下培养的细胞培养基中，一种假定与纤连蛋白相关的高分子量蛋白质明显减少。这些结果表明，衣霉素会干扰一种或多种细胞表面糖蛋白的插入或功能。这种细胞表面变化可能会影响许多细胞特性，包括附着、细胞形状以及某些凝集素的凝集性。
