Radiation-induced signaling pathways that promote cancer cell survival (Review)

被引:160
作者
Hein, Ashley L. [1 ]
Ouellette, Michel M. [1 ]
Yan, Ying [1 ]
机构
[1] Univ Nebraska Med Ctr, Eppley Inst Res Canc & Allied Dis, Omaha, NE 68198 USA
关键词
radiation therapy; signaling pathways; cell cycle checkpoint; DNA repair; cell survival; EPIDERMAL-GROWTH-FACTOR; DOUBLE-STRAND BREAK; DNA-DAMAGE CHECKPOINT; GLYCOGEN-SYNTHASE KINASE-3-BETA; HUMAN TUMOR-CELLS; IONIZING-RADIATION; FACTOR RECEPTOR; TYROSINE PHOSPHORYLATION; INDUCED APOPTOSIS; FEEDBACK-REGULATION;
D O I
10.3892/ijo.2014.2614
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Radiation therapy is a staple cancer treatment approach that has significantly improved local disease control and the overall survival of cancer patients. However, its efficacy is still limited by the development of radiation resistance and the presence of residual disease after therapy that leads to cancer recurrence. Radiation impedes cancer cell growth by inducing cytotoxicity, mainly caused by DNA damage. However, radiation can also simultaneously induce multiple pro-survival signaling pathways, such as those mediated by AKT, ERK and ATM/ATR, which can lead to suppression of apoptosis, induction of cell cycle arrest and/or initiation of DNA repair. These signaling pathways act conjointly to reduce the magnitude of radiation-induced cytotoxicity and promote the development of radioresistance in cancer cells. Thus, targeting these pro-survival pathways has great potential for the radiosensitization of cancer cells. In the present review, we summarize the current literature on how these radiation-activated signaling pathways promote cancer cell survival.
引用
收藏
页码:1813 / 1819
页数:7
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