论文部分内容阅读
腺苷酸活化蛋白激酶(AMP activated protein kinase,AMPK),是细胞能量代谢感受器,在维持细胞能量平衡中发挥重要作用,与肿瘤的发生发展有密切关系。活化的AMPK通过抑制哺乳动物雷帕霉素靶蛋白(mammalian target of rapamycin,m TOR)抑制蛋白质合成、激活细胞周期检查点如激活p53及周期依赖性蛋白激酶(CDK)的抑制因子p21~(cip1)阻滞细胞周期进程,从而抑制细胞生长。近年研究发现,电离辐射在癌细胞中通过共济失调毛细血管扩张突变基因(ATM)激活AMPK并介导信号转导,活化p53-p21~(cip1)信号并抑制m TOR通路。并且,联合AMPK激活剂可调节肿瘤细胞的辐射敏感性。本文就AMPK信号通路在肿瘤放疗方面的最新研究进展进行综述。
AMP activated protein kinase (AMPK), a cell energy metabolism receptor, plays an important role in maintaining cellular energy balance and is closely related to tumorigenesis and development. Activated AMPK inhibits protein synthesis by inhibiting the mammalian target of rapamycin (mTOR), activating cell cycle checkpoints such as the inhibitor of p53 and cyclin-dependent kinase (CDK) p21 ~ (cip1 ) Block cell cycle progression and thus inhibit cell growth. In recent years, it has been found that ionizing radiation activates AMPK in cancer cells via ataxia telangiectasia mutated gene (ATM) and mediates signal transduction, activating p53-p21 ~ (cip1) signal and inhibiting mTOR pathway. In addition, AMPK activators can modulate the radiosensitivity of tumor cells. This article reviews the recent progress of AMPK signaling pathway in tumor radiotherapy.