Fishman M, Gunther G
Cell Immunol. 1986 Jul;100(2):374-88. doi: 10.1016/0008-8749(86)90037-7.
Activated macrophages can recognize, bind to, and lyse tumor cells in an antibody-independent manner. We have found that tumor cells pretreated with phorbol esters are markedly less susceptible to macrophage-mediated cytolysis, although the initial binding step is unaffected. Tumor cells preincubated with tumor-promoting phorbol esters (10(-8)-10(-6) M) were rendered resistant to macrophage kill whereas non-tumor-promoting derivatives were inactive in protecting tumor cells against cytolysis. Inhibition of [3H]phorbol-12,13-dibutyrate binding by other phorbol esters correlated with their potency as tumor promoters and their ability to render tumor cells resistant to macrophage killing. The role of protein kinase C as the receptor to phorbol esters was implicated by inhibition of PDBu binding by phenothiazine derivatives. This suggests a possible mechanism for the resistance of phorbol ester-treated tumor cells to macrophage-mediated cytolysis.
活化的巨噬细胞能够以抗体非依赖的方式识别、结合并裂解肿瘤细胞。我们发现，用佛波酯预处理的肿瘤细胞对巨噬细胞介导的细胞溶解明显不那么敏感，尽管初始结合步骤不受影响。与促肿瘤佛波酯（10^(-8)-10^(-6) M）预孵育的肿瘤细胞对巨噬细胞杀伤产生抗性，而非促肿瘤衍生物在保护肿瘤细胞免受细胞溶解方面无活性。其他佛波酯对[3H]佛波-12,13-二丁酸酯结合的抑制作用与其作为肿瘤促进剂的效力及其使肿瘤细胞对巨噬细胞杀伤产生抗性的能力相关。吩噻嗪衍生物对PDBu结合的抑制暗示了蛋白激酶C作为佛波酯受体的作用。这提示了佛波酯处理的肿瘤细胞对巨噬细胞介导的细胞溶解产生抗性的一种可能机制。
