期刊
BIOMOLECULES
卷 5, 期 3, 页码 1912-1937出版社
MDPI
DOI: 10.3390/biom5031912
关键词
checkpoint; DNA damage response; replication stress; cancer; inhibitor; ATM; ATR; Chk1; Wee1; p53
资金
- Grant agency of the Czech Republic [14-34264S]
- Ministry of Education Youth and Sports [CZ09]
- Grant Agency of Charles University [836613]
Cancer treatments such as radiotherapy and most of the chemotherapies act by damaging DNA of cancer cells. Upon DNA damage, cells stop proliferation at cell cycle checkpoints, which provides them time for DNA repair. Inhibiting the checkpoint allows entry to mitosis despite the presence of DNA damage and can lead to cell death. Importantly, as cancer cells exhibit increased levels of endogenous DNA damage due to an excessive replication stress, inhibiting the checkpoint kinases alone could act as a directed anti-cancer therapy. Here, we review the current status of inhibitors targeted towards the checkpoint effectors and discuss mechanisms of their actions in killing of cancer cells.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据