摘要
内质网应激(endoplasmic reticulum stress, ERS)是细胞受到损伤因素(低氧、低PH、低营养等)作用时,Ca^(2+)平衡紊乱和蛋白质超负荷聚集在内质网所引发的反应。在应激条件下维持新生肽链正确折叠,是肿瘤细胞在低氧、酸中毒等应激环境中保持增殖和抗凋亡的关键因素。本文就内质网应激发生时细胞存活保护机制与肿瘤发生的关系进行综述。
Endoplasmic reticulum stress （ERS） is the response of cells to injury factors （hypoxia, low pH, low nutrients, etc.） leading to disorder of Ca2＋ balance and overload accumulation of protein in the endoplas- mic reticulum. Maintenance of nascent synthetic peptide folding correctly plays a key role in promoting tumor growth and anti-apoptosis in ERS, which induced by stress environment such as hypoxia, acidosis. Here we review the relationship between cell survive mechanisms in ERS and tumor development.
作者
张旭明
王胜超
黄尤光
ZHANG Xuming;WANG Shengchao;HUANG Youguang(Yunnan Cancer Hospital/The Third Affiliated Hospital of Kunming Medical University,Kunming 650118,China;Cancer Institute,The Third Affiliated Hospital of Kunming Medical University,Kunming 650118,China)
出处
《生命的化学》
CAS
CSCD
2018年第5期743-748,共6页
Chemistry of Life
基金
国家自然科学基金项目(81660417)
关键词
内质网应激
未折叠蛋白反应
肿瘤
凋亡
靶向治疗
endoplasmic reticulum stress
unfolded protein response
tumors
apoptosis
targeted therapy
