Iseki S, Ebina T, Ishida N
Cancer Res. 1980 Oct;40(10):3786-91.
Caffeine was found to suppress the cell cycle effects of the cancer chemotherapeutic agent neocarzinostatin (NCS). When caffeine was added together with NCS to the culture of HeLa-S3 cells, NCS-induced inhibition of DNA synthesis and of mitosis was markedly reduced in the presence of caffeine. Theophylline was also effective, but N6, O2'-dibutyryl cyclic adenosine 3':5'-monophosphate was not. The caffeine-caused reduction of cell cycle effects was also observed in several other cancer chemotherapeutic agents, including bleomycin and Adriamycin. In contrast, the single-strand scission of cellular DNA and the final cell lethality induced by NCS were not affected by caffeine. These results suggest that the mechanism by which NCS inhibits the cell cycle traverse involves a kind of cell damage which is repairable in a manner promoted by caffeine and hence is different from single-strand scission of DNA. Such a mechanism might be common to the cell cycle effects of X-irradiation and several cancer chemotherapeutic agents including NCS.
人们发现咖啡因可抑制癌症化疗药物新制癌菌素（NCS）的细胞周期效应。当咖啡因与NCS一起添加到HeLa - S3细胞培养物中时，在咖啡因存在的情况下，NCS诱导的DNA合成抑制和有丝分裂抑制明显降低。茶碱也有效果，但N6, O2'-二丁酰环腺苷3':5'-单磷酸没有效果。在包括博来霉素和阿霉素在内的其他几种癌症化疗药物中也观察到了咖啡因引起的细胞周期效应降低。相比之下，细胞DNA的单链断裂以及NCS诱导的最终细胞致死率不受咖啡因影响。这些结果表明，NCS抑制细胞周期进程的机制涉及一种可被咖啡因促进的方式修复的细胞损伤，因此不同于DNA的单链断裂。这种机制可能是X射线照射以及包括NCS在内的几种癌症化疗药物的细胞周期效应所共有的。
