DNA非同源末端连接与肿瘤的发生及治疗

摘要

DNA双链断裂是真核生物最严重也是最致命的DNA损伤类型,如果无法及时修复就可能启动细胞的凋亡,若是错误修复将导致基因突变或基因组不稳定性,最终会导致肿瘤的产生.非同源末端连接途径作为哺乳动物修复双链断裂的主要机制,它的功能不仅对维持基因组的完整性和细胞的稳定性有重要作用,而且和肿瘤治疗疗效有着密切相关性,修复活性的抑制可以很大程度地提高治疗的敏感性.该文综述了非同源末端连接途径在肿瘤的发生及治疗上的重要作用和机制.%The DNA double-strand break ( DSB ) is one of the most lethal and mutagenic DNA damages in eukaryotes.If DSBs can not be repaired in time,the cells will be induced into apoptosis.If it is erroneously repaired,the cells will result in genome instability which in turn drive tumorigenesis.As the major mechanism for repairing DNA DSBs in mammalian cells,non-homologous end joining ( NHEJ )plays an important role in maintenance of the genome stability,and has close relationsip to the efficacy of tumor treatment.The therapeutic sensitivity will be effectively promoted when the NHEJ activity of cells is inhibited.This review is focused on the role of NHEJ in tumorigenesis and cancer treatment.