Role of epidermal growth factor receptor in DNA damage repair  

作　　者：LU JingChen YANG LiFang TAO YongGuang SUN LunQuan CAO Ya 

机构地区：[1]Key Laboratory of Carcinogenesis of Chinese Ministry of Public Health, Key Laboratory of Carcinogenesis and Cancer Invasion of Chinese Ministry of Education, Cancer Research Institute, Xiangya School of Medicine, Central South University, Changsha 410078, China [2]Department of Medical Oncology, Xiangya Hospital, Central South University, Changsha 410008, China

出　　处：《Chinese Science Bulletin》2011年第30期3132-3137,共6页

基　　金：supported by the National High Technology Research and Development Program of China (2009AA02Z403);the National Natural Science Foundation of China (30873010 and 81072220)

摘　　要：Many human tumor cells are characterized by overexpression or mutation of epidermal growth factor receptor (EGFR). Emerging evidence indicates that EGFR, as well as some of its downstream components, can translocate to the nucleus and play roles in transcriptional regulation, signaling conduction and repair of DNA double strands breaks (DSBs). EGFR in its nuclear manifestation promotes DSB repair by interacting with proteins including DNA-PK, ATM, Rad51 and BRCA1, involved in DSB repair, via the PI3K-Akt and Ras-Raf-MAPK pathways. DNA damage repair in tumor cells is emerging as an attractive target in radiotherapy and chemotherapy. Interruption of EGFR functions, or those of its downstream components, presents a promising strategy for confounding DNA damage repair in tumor cells.Many human tumor cells are characterized by overexpression or mutation of epidermal growth factor receptor （EGFR）. Emerging evidence indicates that EGFR, as well as some of its downstream components, can translocate to the nucleus and play roles in transcriptional regulation, signaling conduction and repair of DNA double strands breaks （DSBs）. EGFR in its nuclear manifesta- tion promotes DSB repair by interacting with proteins including DNA-PK, ATM, Rad51 and BRCA1, involved in DSB repair, via the PI3K-Akt and Ras-Raf-MAPK pathways. DNA damage repair in tumor cells is emerging as an attractive target in radiotherapy and chemotherapy. Interruption of EGFR functions, or those of its downstream components, presents a promising strategy for confounding DNA damage repair in tumor cells.

关 键 词：表皮生长因子受体 DNA损伤修复 肿瘤细胞 MAPK途径 双链断裂 自动柜员机 BRCA1 过度表达 

分 类 号：R730.2[医药卫生—肿瘤]