Boehm T L, Drahovsky D
Cancer Res. 1982 Apr;42(4):1537-40.
When mouse P815 mastocytoma cells are cultured in the presence of 1-beta-D-arabinofuranosylcytosine (ara-C), a dose-dependent inhibition of cell proliferation and DNA synthesis can be observed. The DNA synthesized in the presence of ara-C is more highly enzymatically methylated than that of controls as measured by conversion of incorporated [14C]deoxycytidine-derived radioactivity into 5-methylcytosines. Analysis of DNAs by means of the bacterial restriction enzyme HpaII and its isoschizomer MspI revealed an aberrant DNA methylation pattern after ara-C treatment. The hypermethylation of DNA persisted also in the cell cycle following the treatment in the absence of ara-C. No such changes in DNA methylation patterns following ara-C treatment were observed in P815/ara-C, a subclone of P815 cells resistant to ara-C.
当小鼠P815肥大细胞瘤细胞在1-β-D-阿拉伯呋喃糖基胞嘧啶（ara-C）存在的情况下进行培养时，可以观察到细胞增殖和DNA合成受到剂量依赖性抑制。通过将掺入的[14C]脱氧胞苷衍生的放射性转化为5-甲基胞嘧啶来测量，在ara-C存在下合成的DNA比对照的DNA具有更高的酶促甲基化水平。通过细菌限制酶HpaII及其同裂酶MspI对DNA进行分析，结果显示ara-C处理后DNA甲基化模式异常。在不存在ara-C的情况下进行处理后，DNA的高甲基化在细胞周期中仍然持续存在。在对ara-C具有抗性的P815细胞亚克隆P815/ara-C中，未观察到ara-C处理后DNA甲基化模式的此类变化。
