内质网应激与髓细胞白血病耐药关系的新进展

Advance in relationship between endoplasmic reticulum stress and myeloid leukemia resistance

内质网是蛋白质合成、折叠和修饰,脂质合成和钙储存的关键细胞器。不同的细胞应激,导致未折叠和错误折叠的蛋白质在内质网中累积,从而发生内质网应激(ERS)反应。在髓细胞白血病(ML)中,ERS常以激活未折叠蛋白反应(UPR)和自噬的方式,缓解ERS反应,帮助ML细胞逃避长时间ERS诱导的细胞死亡作用。因此,UPR和自噬可能是ERS调控ML发生耐药的重要机制。笔者通过ERS概述、ERS与ML耐药、ERS介导的自噬与ML耐药等方面的研究进展,就ERS与ML耐药的关系进行阐述。

The endoplasmic reticulum is a critical organelle for synthesis,folding and modification of protein,lipid synthesis and calcium storage.Unfolded or misfolded proteins accumulate because of different cellular stress resulting in endoplasmic reticulum stress(ERS).In myeloid leukemia(ML),ERS usually activates the unfolded protein response(UPR)and autophagy which can help tumor cells escaping cell death induced by ERS.Therefore,UPR and autophagy may be important mechanisms in regulation of ML resistance.This article summarizes relationship between ERS and ML resistance in terms of ERS overview,ERS and ML resistance,as well as relationship between autophagy caused by ERS and ML resistance.