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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Defective double-strand DNA break repair and chromosomal translocations by MYC overexpression.
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Defective double-strand DNA break repair and chromosomal translocations by MYC overexpression.

机译：有缺陷的双链DNA断裂修复和MYC过表达引起的染色体易位。

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摘要

DNA repair mechanisms are essential for the maintenance of genomic integrity. Disruption of gene products responsible for DNA repair can result in chromosomal damage. Improperly repaired chromosomal damage can result in the loss of chromosomes or the generation of chromosomal deletions or translocations, which can lead to tumorigenesis. The MYC protooncogene is a transcription factor whose overexpression is frequently associated with human neoplasia. MYC has not been previously implicated in a role in DNA repair. Here we report that the overexpression of MYC disrupts the repair of double-strand DNA breaks, resulting in a several-magnitude increase in chromosomal breaks and translocations. We found that MYC inhibited the repair of gamma irradiation DNA breaks in normal human cells and blocked the repair of a single double-strand break engineered to occur in an immortal cell line. By spectral karyotypic analysis, we found that MYC even within one cell division cycle resulted in a several-magnitude increase in the frequency of chromosomal breaks and translocations in normal human cells. Hence, MYC overexpression may be a previously undescribed example of a dominant mutator that may fuel tumorigenesis by inducing chromosomal damage.
机译：DNA修复机制对于维持基因组完整性至关重要。破坏负责DNA修复的基因产物可能会导致染色体损伤。修复不当的染色体损伤会导致染色体丢失或染色体缺失或易位，从而导致肿瘤的发生。 MYC原癌基因是一种转录因子，其过度表达通常与人类肿瘤形成有关。 MYC以前并未涉及DNA修复的作用。在这里，我们报道MYC的过表达破坏了双链DNA断裂的修复，导致染色体断裂和易位增加了几倍。我们发现MYC抑制了正常人细胞中伽马射线DNA断裂的修复，并阻止了改造成在永生细胞系中发生的单个双链断裂的修复。通过光谱核型分析，我们发现即使在一个细胞分裂周期内，MYC也会导致正常人细胞中染色体断裂和易位的频率增加几倍。因此，MYC过表达可能是一个显性突变体的先前未描述的例子，该显性突变体可通过诱导染色体损伤来助长肿瘤发生。

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