DNA修复
DNA损伤
生物
细胞生物学
癌症研究
细胞周期
细胞周期检查点
细胞周期蛋白B1
癌变
细胞周期蛋白依赖激酶1
癌症
DNA
遗传学
作者
Yan Wang,Huizhen Sun,Ziliang Wang,Mingming Liu,Zihao Qi,Jiao Meng,Jianmin Sun,Gong Yang
出处
期刊:Tumor Biology
[SAGE]
日期:2013-11-25
卷期号:35 (4): 2831-2836
被引量:25
标识
DOI:10.1007/s13277-013-1393-8
摘要
It is well-known that overexpression of Aurora-A promotes tumorigenesis, but the role of Aurora-A in the development of cancer has not been fully investigated. Recent studies indicate that Aurora-A may confer cancer cell chemo- and radioresistance through dysregulation of cell cycle progression and DNA damage response. Direct evidences from literatures suggest that Aurora-A inhibits pRb, p53, p21waf1/cip1, and p27cip/kip but enhances Plk1, CDC25, CDK1, and cyclin B1 to repeal cell cycle checkpoints and to promote cell cycle progression. Other studies indicate that Aurora-A suppresses BRCA1, BRCA2, RAD51, poly(ADP ribose) polymerase (PARP), and gamma-H2AX to dysregulate DNA damage response. Aurora-A may also interact with RAS and Myc to control DNA repair indirectly. In this review, we summarized the potential role of Aurora-A in DNA repair from the current literatures and concluded that Aurora-A may function as a DNA repair modulator to control cancer cell radio- and chemosensitivity, and that Aurora-A-associated DNA repair molecules may be considered for targeted cancer therapy.
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