Pincus S M, Beckman B S, George W J
Biochem Biophys Res Commun. 1984 Dec 14;125(2):491-9. doi: 10.1016/0006-291x(84)90567-9.
The effects of diacylglycerols and phospholipase C on dimethylsulfoxide (DMSO)-induced differentiation were investigated in Friend erythroleukemic cells (FELC). Greater than 80% of cells become benzidine-positive when incubated with 1.5% DMSO. The tumor promoter, 12-O-tetradecanoyl-phorbol-13-acetate (TPA), inhibits DMSO-induced differentiation in FELC. Diacylglycerols were found to inhibit DMSO-induced differentiation dose responsively with the order of potency being 1-oleoyl-2-acetylglycerol (OAG) greater than dicaprylin greater than dilaurin greater than diolein. Phospholipase C which releases endogenous diacylglycerols from membrane phospholipids also inhibited DMSO-induced differentiation dose responsively. These results support the hypothesis that diacylglycerols can have effects similar to tumor promoters and suggest that protein kinase C may be a common mechanism for tumor promotion.
在弗氏红白血病细胞（FELC）中研究了二酰甘油和磷脂酶C对二甲基亚砜（DMSO）诱导分化的影响。当与1.5% DMSO孵育时，超过80%的细胞会变成联苯胺阳性。肿瘤促进剂12-O-十四烷酰佛波醇-13-乙酸酯（TPA）可抑制FELC中DMSO诱导的分化。发现二酰甘油以剂量依赖方式抑制DMSO诱导的分化，效力顺序为1-油酰基-2-乙酰甘油（OAG）大于二辛脂大于二月桂精大于二油精。从膜磷脂释放内源性二酰甘油的磷脂酶C也以剂量依赖方式抑制DMSO诱导的分化。这些结果支持了二酰甘油可具有与肿瘤促进剂类似作用的假说，并表明蛋白激酶C可能是肿瘤促进的共同机制。
