内质网应激与肿瘤细胞的凋亡  

Endoplasmic reticulum stress and apoptosis of tumor cells

作　　者：原玉芬[1] 杨惠玲[1] 

机构地区：[1]中山大学中山医学院病理生理学教研室,广东广州510080

出　　处：《分子诊断与治疗杂志》2010年第2期128-134,共7页Journal of Molecular Diagnostics and Therapy

基　　金：国家自然科学基金项目(NO:30670627)

摘　　要：内质网(endoplasmic reticulum,ER)是重要的细胞器,是蛋白质合成、折叠、组装和钙离子储存等的场所。多种生理和病理条件下,如缺氧、氧化还原状态的改变等可干扰内质网的功能,并引起未折叠蛋白在ER中堆积,产生内质网应激(endoplasmic reticulum stress,ERS)。虽然ERS可诱导细胞的生存,然而长时间过强的ERS可诱导细胞凋亡,即内质网应激反应性凋亡。Endoplasmic reticulum is an important organelle that has many function such as calcium storage protein synthesis,folding and assembly. A variety of injuries,including hypoxia changes in redox state,may interfere with the function of the endoplasmic reticulum and cause unfolded protein accumulation in the ER which result in endoplasmic reticulum stress（ERS）. Although ERS can induce cell survival,if it effects too strong or for a long time,ERS may cause apoptosis,i.e. endoplasmic reticulum stress-induced apoptosis.

关 键 词：内质网应激 未折叠蛋白反应 肿瘤 凋亡 

分 类 号：R730.2[医药卫生—肿瘤]