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放射线主要通过导致细胞DNA双链断裂(DSB)而起到杀死肿瘤细胞的作用,但细胞都有不同程度的DSB修复能力,研究证实DSB修复水平与细胞放射敏感性关系密切。在人类细胞内有2种DSB修复途径:一种是以DNA依赖蛋白激酶(DNA-PK)复合物为主的非同源末端连接(NHEJ)修复,另一种是以毛细血管扩张性共济失调症突变蛋白(ATM)为主的同源重组(HR)修复在人体内,NHEJ修复是最主要的修复途径,DNA依赖蛋白激酶催化亚单位(DNA-PKcs)是DNA-PK复合物的主要功能单位。DNA-PKcs的激酶活性是NHEJ修复所必须的,其在DSB修复中起核心作用近年来的研究显示ATM、DNA-PKcs蛋白表达水平与肿瘤放射敏感性有关。该综述将有关ATM、DNA-PKcs的功能、在肿瘤组织中的表达及与肿瘤放射敏感性关系的研究进行简要回顾。
Radiation mainly plays a role in killing tumor cells by causing DNA double-strand break (DSB) of cells, but the cells have different degrees of DSB repair ability. Studies confirm that the level of DSB repair is closely related to cell radiosensitivity. There are two pathways for DSB repair in human cells: one is a non-homologous end-junction (NHEJ) repair based on a DNA-PK complex, and the other is a telangiectasia Mitotic Mutant Protein (ATM) -based Homologous Recombination (HR) Repair In humans, NHEJ repair is the most important repair pathway and the DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is the major component of the DNA-PK complex Functional units. The kinase activity of DNA-PKcs, which is essential for NHEJ repair, plays a central role in DSB repair. Recent studies have shown that the expression of ATM and DNA-PKcs is related to tumor radiosensitivity. This review provides a brief review of the studies on the function of ATM, DNA-PKcs, their expression in tumor tissues and the relationship with tumor radiosensitivity.