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首页> 外文期刊>Molecular and Cellular Biology >DNA methylation in 5-aza-2'-deoxycytidine-resistant variants of C3H 10T1/2 C18 cells.
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DNA methylation in 5-aza-2'-deoxycytidine-resistant variants of C3H 10T1/2 C18 cells.

机译：C3H 10T1 / 2 C18细胞的5-氮杂2'-脱氧胞苷抗性变异体中的DNA甲基化。

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摘要

A cell line (T17) was derived from C3H 10T1/2 C18 cells after 17 treatments with increasing concentrations of 5-aza-2'-deoxycytidine. The T17 cell line was very resistant to the cytotoxic effects of 5-aza-2'-deoxycytidine, and the 50% lethal dose for 5-aza-2'-deoxycytidine was ca. 3 microM, which was 30-fold greater than that of the parental C3H 10T1/2 C18 cells. Increased drug resistance was not due to a failure of the T17 cell line to incorporate 5-aza-2'-deoxycytidine into DNA. The cells were also slightly cross-resistant to 5-azacytidine. The percentage of cytosines modified to 5-methylcytosine in T17 cells was 0.7%, a 78% decrease from the level of 3.22% in C3H 10T1/2 C18 cells. The DNA cytosine methylation levels in several clones isolated from the treated lines were on the order of 0.7%, and clones with methylation levels lower than 0.45% were not obtained even after further drug treatments. These highly decreased methylation levels appeared to be unstable, and DNA modification increased as the cells divided in the absence of further drug treatment. The results suggest that it may not be possible to derive mouse cells with vanishingly low levels of 5-methylcytosine and that considerable de novo methylation can occur in cultured lines.
机译：用浓度增加的5-氮杂-2'-脱氧胞苷处理17次后，来自C3H 10T1 / 2 C18细胞的细胞系（T17）。 T17细胞系对5-氮杂2'-脱氧胞苷的细胞毒性作用非常有抵抗力，而5-氮杂2'-脱氧胞苷的50％致死剂量为。 3 microM，比亲代C3H 10T1 / 2 C18细胞大30倍。耐药性的提高并不是由于T17细胞系未能将5-氮杂2'-脱氧胞苷掺入DNA中所致。细胞还对5-氮杂胞苷略有交叉抗性。在T17细胞中修饰为5-甲基胞嘧啶的胞嘧啶百分比为0.7％，比C3H 10T1 / 2 C18细胞的3.22％水平降低了78％。从经处理的品系分离的几个克隆中，DNA胞嘧啶甲基化水平约为0.7％，即使经过进一步的药物处理，也无法获得甲基化水平低于0.45％的克隆。这些高度降低的甲基化水平似乎不稳定，并且在没有进一步药物治疗的情况下，随着细胞分裂，DNA修饰增加。结果表明，可能无法获得5-甲基胞嘧啶水平极低的小鼠细胞，并且在培养的系中可能发生大量的从头甲基化。

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