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首页> 外文期刊>Cell cycle >High doses of SN1 type methylating agents activate DNA damage signaling cascades that are largely independent of mismatch repair.
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High doses of SN1 type methylating agents activate DNA damage signaling cascades that are largely independent of mismatch repair.

机译：高剂量的SN1型甲基化剂可激活DNA损伤信号传导级联反应，而该级联反应很大程度上与错配修复无关。

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摘要

Methylating agents of the SN1 type represent an important class of cancer chemotherapeutics. Efficient killing by clinically-relevant doses of these agents requires cell division and low levels or absence of the repair enzyme methylguanine methyl transferase (MGMT). The process requires also an active mismatch repair (MMR) system, as treatment of cells with the prototypic methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) could be shown to trigger a delayed cell cycle arrest, which was absolutely MMR-dependent. We now show that DNA damage signaling activated by high doses of MNNG is very rapid and largely MMR-independent. However, the MMR system still contributes towards cell killing, as MMR deficiency favors the long-term survival of the cells, albeit to a substantially smaller extent than when low MNNG concentrations are deployed.
机译：SN1型甲基化剂代表了癌症化学治疗的重要一类。通过临床相关剂量的这些药剂有效杀灭需要细胞分裂，并且水平低或缺乏修复酶甲基鸟嘌呤甲基转移酶（MGMT）。该过程还需要一个主动错配修复（MMR）系统，因为用原型甲基化剂N-甲基-N'-硝基-N-亚硝基胍（MNNG）处理细胞可能会触发延迟的细胞周期停滞，这是绝对依赖于MMR。我们现在显示，由高剂量的MNNG激活的DNA损伤信号传导非常迅速，并且在很大程度上与MMR无关。但是，MMR系统仍然有助于细胞杀伤，因为MMR缺乏有利于细胞的长期存活，尽管其程度远低于低MNNG浓度时的存活率。

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