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首页> 外文期刊>Cell cycle >XRCC3 depletion induces spontaneous DNA breaks and p53-dependent cell death.
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XRCC3 depletion induces spontaneous DNA breaks and p53-dependent cell death.

机译：XRCC3耗尽诱导自发DNA断裂和p53依赖性细胞死亡。

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In vertebrate cells, Xrcc3 initiates the repair of exogenous induced-DNA breaks during S and G(2)/M phases of the cell cycle by homologous recombination. However, much less is known of the role of Xrcc3 in the response to spontaneous DNA breaks. Using a siRNA approach, we show that depletion of XRCC3 inhibits the proliferation of MCF7 breast cancer cells. This inhibition of replication coincides with the accumulation of DNA breaks, as shown by the comet assay. Cell cycle specific analysis of gammaH2AX expression shows that S and G2/M phase cells express the highest fraction of gammaH2AX positive cells. This is consistent with replication-dependent accumulation of DNA breaks and deficient homologous recombination. While the induction of gammaH2AX is followed by cell death in parental cells, a p53 knockdown derivative becomes more resistant to XRCC3 depletion-induced death without changes in the levels of gammaH2AX. These results show that XRCC3 is required for the proliferation of MCF7 cells, and that decrease in its expression leads to the accumulation of DNA breaks and the induction of p53-dependent cell death.
机译：在脊椎动物细胞中，Xrcc3通过同源重组启动细胞周期的S和G（2）/ M阶段的外源诱导DNA断裂的修复。但是，人们对Xrcc3在对自发DNA断裂的反应中的作用知之甚少。使用siRNA方法，我们显示XRCC3的耗竭抑制MCF7乳腺癌细胞的增殖。如彗星试验所示，这种复制抑制作用与DNA断裂的积累相吻合。对gammaH2AX表达的细胞周期特异性分析表明，S和G2 / M期细胞表达最高比例的gammaH2AX阳性细胞。这与DNA断裂的复制依赖性积累和缺陷的同源重组相一致。虽然在亲代细胞中诱导了gammaH2AX的死亡后，p53敲低衍生物变得对XRCC3耗尽诱导的死亡更具抗性，而gammaH2AX的水平却没有变化。这些结果表明，XRCC3是MCF7细胞增殖所必需的，其表达下降会导致DNA断裂的积累并诱导p53依赖性细胞死亡。

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