Hoshino J, Frahm J, Kröger H
Biochem Biophys Res Commun. 1987 Jan 30;142(2):468-74. doi: 10.1016/0006-291x(87)90298-1.
The exposure of freshly isolated, activity growing Ehrlich ascites tumor cells to the antileukemic agent 5-azacytidine and its analogs, 5-azacytosine (but not 6-azacytosine), 5-aza-2'-deoxycytidine and, in particular, 5-fluorocytidine in the serum-free medium caused a time- and dose-dependent suppression of the nuclear ADP-ribosyltransferase activity. The azacytidine suppression was apparently dependent on the cellular activity of DNA synthesis but not related to the nuclear activity of DNA methylation, indicating the 5-azacytidine incorporation into DNA, but not drug-induced hypomethylation of DNA, being responsible for the 5-azacytidine-suppression of chromatin-bound ADP-ribosyltransferase.
将新鲜分离的、处于活性生长状态的艾氏腹水瘤细胞暴露于抗白血病药物5-氮杂胞苷及其类似物5-氮杂胞嘧啶(但不包括6-氮杂胞嘧啶)、5-氮杂-2'-脱氧胞苷,特别是在无血清培养基中的5-氟胞苷,会导致核ADP-核糖基转移酶活性出现时间和剂量依赖性抑制。氮杂胞苷的抑制作用显然依赖于DNA合成的细胞活性,但与DNA甲基化的核活性无关,这表明5-氮杂胞苷掺入DNA,而非药物诱导的DNA低甲基化,是染色质结合的ADP-核糖基转移酶受5-氮杂胞苷抑制的原因。