聚（ADP-核糖）合成抑制剂对体外恶性转化的抑制作用。
Inhibition of malignant transformation in vitro by inhibitors of poly(ADP-ribose) synthesis.
作者信息
Borek C, Morgan W F, Ong A, Cleaver J E
出版信息
Proc Natl Acad Sci U S A. 1984 Jan;81(1):243-7. doi: 10.1073/pnas.81.1.243.
Abstract
Malignant transformation in vitro of hamster embryo cells and mouse C3H 10T 1/2 cells by x-rays, ultraviolet light, and chemical carcinogens was inhibited by benzamide and by 3-aminobenzamide at concentrations that are specific for inhibition of poly(ADP-ribose) formation. These compounds slow the ligation stage of repair of x-ray and alkylation damage but not of ultraviolet light damage. At high concentrations they also inhibited de novo synthesis of DNA purines and DNA methylation by S-adenosylmethionine. The suppression of transformation by the benzamides is in striking contrast to their reported effectiveness in enhancing sister chromatid exchange, mutagenesis, and killing in cells exposed to alkylating agents. Our results suggest that mechanisms regulating malignant transformation are different from those regulating DNA repair, sister chromatid exchange, and mutagenesis and may be associated with changes in gene regulation and expression caused by alterations in poly(ADP-ribosyl)ation.
摘要
苯甲酰胺和3-氨基苯甲酰胺在抑制聚（ADP-核糖）形成的特定浓度下，可抑制仓鼠胚胎细胞和小鼠C3H 10T 1/2细胞经X射线、紫外线和化学致癌物诱导的体外恶性转化。这些化合物减缓了X射线和烷基化损伤修复的连接阶段，但不影响紫外线损伤的修复。在高浓度时，它们还抑制DNA嘌呤的从头合成以及S-腺苷甲硫氨酸介导的DNA甲基化。苯甲酰胺对转化的抑制作用与它们在增强暴露于烷化剂的细胞中的姐妹染色单体交换、诱变和杀伤作用方面所报道的有效性形成了鲜明对比。我们的结果表明，调节恶性转化的机制不同于调节DNA修复、姐妹染色单体交换和诱变的机制，可能与聚（ADP-核糖基）化改变引起的基因调控和表达变化有关。
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