细胞周期检验点与肿瘤发生之间关系的研究进展

DNA损伤反应引起的基因组不稳定性并不足以导致肿瘤发生，还需要一些协同突变促进肿瘤的生长或存活，因此，基因组结构不稳定和周期检验点突变失活是肿瘤发生的重要因素。与正常细胞不同，肿瘤细胞中细胞周期检验点反应缺陷，当肿瘤细胞遭受基因毒药物损伤时，可通过激活周期检验点反应阻滞细胞周期进程，加强损伤修复，导致耐药表型的产生。因此，寻找特异性的检验点抑制剂来加强化疗药物或辐射对肿瘤细胞的杀伤效应，已成为肿瘤治疗的一个研究方向。

Progress of Relationship Between Cell-Cycle Checkpoint and Tumorigenesis

Genomic instability caused by DNA damages is not enough to result in tumorigenesis, and some coordinate mutation is required for tumor growth and survival. Hence, both genomic instability and cell-cycle checkpoint dysfunction are critical factors for tumorigenesis. Different from normal cells, tumor cells always have some checkpoint defects. When suffering genotoxicity, tumor cells can activate cell-cycle checkpoints to block cell-cycle progress, which enhances damage repairing and leads to resistance phenotype. For the reasons above, looking for specific checkpoint inhibitor to intensify tumor-cell lethal effects of chemotherapeutics and radiotherapeutics has already been a new trend for tumor therapy research.