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Science:研究揭示癌细胞修复DNA损伤的新机制

来源:生物谷 2013-12-15 22:37

2013年12月15日讯 /生物谷BIOON/--癌细胞分裂失控过程会造成DNA损伤,但癌症细胞有修复受损DNA的特殊能力。现在科学家们揭示了癌症细胞DNA修复的一种新机制。这些发现是通过使用VTT资深科学家Juha Rantala开发的细胞芯片筛选方法实现的。这项新研究对抗癌药物的发展将产生重大影响,相关研究成果发表在Science杂志上。

新的研究结果部分解释了为什么癌细胞与正常细胞不同,不会死于DNA损伤。现在,科学家们了解了修复机制,他们可以更好地开发药物疗法,针对专门癌细胞。

所发现的DNA修复机制以前没有在人或哺乳动物细胞中被描述。癌细胞利用这一机制来修复DNA损伤,导致激活的癌基因进一步促使失控的DNA复制。运用Juha Rantala开发的细胞微芯片筛选方法发现了参与DNA修复机制的基因,该筛选方法允许一个单一的微芯片能够同时筛选数以万计基因。(生物谷Bioon.com)
 

Break-Induced Replication Repair of Damaged Forks Induces Genomic Duplications in Human Cells

Lorenzo Costantino1,et al.

In budding yeast, one-ended DNA double-strand breaks (DSBs) and damaged replication forks are repaired by break-induced replication (BIR), a homologous recombination pathway that requires the Pol32 subunit of DNA polymerase delta. DNA replication stress is prevalent in cancer, but BIR has not been characterized in mammals. In a cyclin E overexpression model of DNA replication stress, POLD3, the human ortholog of POL32, was required for cell cycle progression and processive DNA synthesis. Segmental genomic duplications induced by cyclin E overexpression were also dependent on POLD3, as were BIR-mediated recombination events captured with a specialized DSB repair assay. We propose that BIR repairs damaged replication forks in mammals, accounting for the high frequency of genomic duplications in human cancers.

 

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