Translesion DNA polymerases and cancer.
Translesion DNA polymerases and cancer.
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DOI：
10.3389/fgene.2012.00174
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发表时间：
2012
影响因子：
3.7
通讯作者：
Reichardt JK
中科院分区：
文献类型：
--
作者：
Makridakis NM;Reichardt JK
DNA修复被认为是肿瘤发生的重要屏障。新发现的跨损伤合成（TLS）领域已经表明，哺乳动物细胞需要不同的聚合酶来有效和准确地绕过DNA损伤。预期突变、表达缺失等对TLS聚合酶活性的干扰会导致暴露于特定致癌物的细胞中突变的累积。此外，几种TLS聚合酶可以调节细胞对化疗剂的敏感性。因此，TLS基因和TLS基因变异可能是有吸引力的药理学和/或药物遗传学靶标。我们在此审查目前的数据，关于主要的TLS聚合酶基因对癌症的潜在贡献，它们与药物的相互作用，并确定感兴趣的领域进行进一步的研究。
DNA repair has been regarded as an important barrier to carcinogenesis. The newly discovered field of translesion synthesis (TLS) has made it apparent that mammalian cells need distinct polymerases to efficiently and accurately bypass DNA lesions. Perturbation of TLS polymerase activity by mutation, loss of expression, etc. is expected to result in the accumulation of mutations in cells exposed to specific carcinogens. Furthermore, several TLS polymerases can modulate cellular sensitivity to chemotherapeutic agents. TLS genes and TLS gene variations may thus be attractive pharmacologic and/or pharmacogenetic targets. We review herein current data with regards to the potential contribution of the primary TLS polymerase genes to cancer, their interaction with pharmacologic agents, and identify areas of interest for further research.