内质网应激在抗肿瘤治疗中的作用及研究进展  

Role and research progress of endoplasmic reticulum stress in anti-tumor therapy

作　　者：王安琪 孙国平[1] WANG An-qi;SUN Guo-ping(Dept of Oncology, the First Affiliated Hospital of Anhui Medical University, Hefei 230022,China)

机构地区：[1]安徽医科大学第一附属医院肿瘤科,安徽合肥230022

出　　处：《中国药理学通报》2021年第12期1643-1647,共5页Chinese Pharmacological Bulletin

基　　金：国家自然科学基金资助项目(No 82072751,81872047,81572430,81272739,81071986)。

摘　　要：在肿瘤的发生、发展及转移过程中,肿瘤细胞经历的缺氧、低糖、酸中毒等应激环境,使肿瘤细胞发生内质网应激,内质网应激启动未折叠蛋白反应使细胞恢复稳态;但当内质网应激超过细胞的存活能力时,则会介导细胞凋亡。该文主要从抑制未折叠蛋白反应介导的促生存通路和诱导持续的内质网应激介导的促死亡通路两个方面,阐述了内质网应激在抗肿瘤治疗中的作用及研究进展,以深入了解内质网应激相关途径与抗肿瘤治疗的关系,希望能为肿瘤治疗提供新思路。In the process of tumor occurrence,development and metastasis,the stress environment experienced by tumor cells such as hypoxia,low glucose,acidosis,can cause tumor cells to undergo endoplasmic reticulum stress(ERS).In order to restore cell homeostasis,ERS initiates the unfolded protein response(UPR).But when ERS exceeds the survival ability of cells,it will mediate cell apoptosis.This article expounds the role of ERS in anti-tumor therapy and its research progress mainly from the two aspects of inhibition of UPR mediated promote survival pathways and induction of ERS mediated death pathways,in order to understand the relationship between ERS-related pathways and anti-tumor treatments,hoping to provide new ideas for tumor treatment.

关 键 词：内质网应激 未折叠蛋白反应 肿瘤 治疗 通路 自噬 

分 类 号：R329.24[医药卫生—人体解剖和组织胚胎学] R341[医药卫生—基础医学]