DNA damage-dependent cell cycle checkpoints and genomic stability
DNA damage-dependent cell cycle checkpoints and genomic stability
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DOI：
10.1089/dna.2006.25.406
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发表时间：
2006-07-01
影响因子：
3.1
通讯作者：
Saito, Toshiyuki
中科院分区：
文献类型：
--
作者：
Ishikawa, Kazuhiro;Ishii, Hideshi;Saito, Toshiyuki
为了响应可能由环境或内源性基因毒性损伤（例如电离或紫外线辐射）、各种化学物质和反应性细胞代谢物引起的基因毒性应激，可以激活减缓或阻止细胞周期进程的细胞周期检查点，从而使细胞能够修复或阻止受损或不完全复制的染色体的传递。检查点机制还可以启动导致细胞凋亡和从组织中去除受损细胞的途径。一方面细胞周期停滞和损伤修复与细胞死亡启动之间的平衡可以确定细胞或DNA损伤是否与细胞存活相容或需要通过细胞凋亡消除细胞。这些过程中的缺陷可能导致对细胞应激的超敏反应，以及对 DNA 损伤、基因组缺陷和细胞凋亡抵抗的敏感性，这些都是癌细胞的特征。在本文中，我们注意到最近对 DNA 损伤依赖性细胞周期检查点的研究，这可能对防止基因组不稳定具有重要意义。
In response to genotoxic stress, which can be caused by environmental or endogenous genotoxic insults such as ionizing or ultraviolet radiation, various chemicals and reactive cellular metabolites, cell cycle checkpoints which slow down or arrest cell cycle progression can be activated, allowing the cell to repair or prevent the transmission of damaged or incompletely replicated chromosomes. Checkpoint machineries can also initiate pathways leading to apoptosis and the removal of a damaged cell from a tissue. The balance between cell cycle arrest and damage repair on one hand and the initiation of cell death, on the other hand, could determine if cellular or DNA damage is compatible with cell survival or requires cell elimination by apoptosis. Defects in these processes may lead to hypersensitivity to cellular stress, and susceptibility to DNA damage, genomic defects, and resistance to apoptosis, which characterize cancer cells. In this article, we have noted recent studies of DNA damage-dependent cell cycle checkpoints, which may be significant in preventing genomic instability.