Rodemann H Peter, Dittmann Klaus, Toulany Mahmoud
Division of Radiobiology & Molecular Environmental Research, Department of Radiation Oncology, Eberhard-Karls University Tuebingen, Germany.
Int J Radiat Biol. 2007 Nov-Dec;83(11-12):781-91. doi: 10.1080/09553000701769970.
Over the last decade evidence has accumulated indicating that cell membrane-bound growth factor receptor of the erbB family and especially the epidermal growth factor receptor EGFR (erbB1) mediates resistance of tumor cells to both chemo- and radiotherapy when mutated or overexpressed. More recently a novel link between EGFR signaling pathways and DNA repair mechanisms, especially non-homologous end joining (NHEJ) repair could be demonstrated. The following review summarizes the current knowledge on the role of EGFR and its downstream signaling pathways in the regulation of cellular radiation response and DNA repair.
The novel findings on radiation-induced EGFR-signaling and its involvement in regulating DNA-double strand break repair need further investigations of the detailed mechanisms involved. The results to be obtained may not only improve our knowledge on basic mechanisms of radiation sensitivity/resistance but also will promote translational approaches to test new strategies for clinically applicable molecular targeting.
在过去十年中，越来越多的证据表明，erbB家族的细胞膜结合生长因子受体，尤其是表皮生长因子受体EGFR（erbB1），在发生突变或过表达时，介导肿瘤细胞对化疗和放疗的抗性。最近，EGFR信号通路与DNA修复机制，尤其是非同源末端连接（NHEJ）修复之间的新联系得到了证实。以下综述总结了关于EGFR及其下游信号通路在调节细胞辐射反应和DNA修复中的作用的当前知识。
关于辐射诱导的EGFR信号及其参与调节DNA双链断裂修复的新发现，需要对所涉及的详细机制进行进一步研究。所获得的结果不仅可能提高我们对辐射敏感性/抗性基本机制的认识，还将促进转化研究方法，以测试临床适用的分子靶向新策略。
