Claspin: From replication stress and DNA damage responses to cancer therapy

被引:8
作者
Azenha, Diana [1 ,2 ,3 ,4 ]
Lopes, Maria Celeste [1 ,2 ,3 ]
Martins, Teresa C. [2 ,3 ,4 ]
机构
[1] Univ Coimbra, Fac Pharm, Coimbra, Portugal
[2] Univ Coimbra, Ctr Neurosci & Cell Biol, Coimbra, Portugal
[3] Univ Coimbra, Inst Biomed Imaging & Life Sci CNC IBILI, Coimbra, Portugal
[4] Portuguese Inst Oncol Coimbra, Coimbra, Portugal
来源
DNA REPAIR | 2019年 / 115卷
关键词
CHECKPOINT KINASE 1; DISRUPTS HOMOLOGOUS RECOMBINATION; SMALL-MOLECULE INHIBITOR; S-PHASE CHECKPOINT; MISMATCH REPAIR; DEPENDENT PHOSPHORYLATION; CHK1; ACTIVATION; PROTEIN-KINASE; OVARIAN-CANCER; FRAGILE SITES;
D O I
10.1016/bs.apcsb.2018.10.007
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Cancer is still one of the major causes of death worldwide. Radiation therapy and chemotherapy remain the main treatment modalities in cancer. These therapies exert their effect mainly through interference with DNA replication and induction of DNA damage. It is believed that one way of improving the efficacy of cancer treatment will be to inhibit the replication stress and DNA damage responses and promote mitotic catastrophe of cancer cells. So far, the majority of the efforts have focused central players of checkpoint responses, such as ATR and CHK1, and DNA damage repair, such as PARPs. Being a key player in the replication stress response, checkpoint activation, and the DNA damage response, Claspin constitutes an attractive therapeutic target in cancer, namely for radio- and chemo-sensitization. In this review, we will go through Claspin functions in the replication stress and DNA damage responses and will discuss how Claspin can be targeted in cancer treatment, as well as the effects of Claspin inhibition.
引用
收藏
页码:203 / 246
页数:44
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