Sodium selenite induces apoptosis by ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction in human acute promyelocytic leukemia NB4 cells

被引：101

作者：

Guan, Liying ^{[1
,2
,3
]}

Han, Binshe ^{[2
,3
]}

Li, Zhushi ^{[2
,3
]}

Hua, Fangyuan ^{[2
,3
]}

Huang, Fang ^{[2
,3
]}

Wei, Wei ^{[2
,3
]}

Yang, Yang ^{[2
,3
]}

Xu, Caimin ^{[2
,3
]}

机构：

[1] Chinese Acad Sci, Key Lab Mol Dev Biol, Inst Genet & Dev Biol, Beijing, Peoples R China

[2] Peking Union Med Coll, Natl Lab Med Mol Biol, Inst Basic Med Sci, Beijing 100021, Peoples R China

[3] Chinese Acad Med Sci, Beijing 100037, Peoples R China

来源：

APOPTOSIS | 2009年 / 14卷 / 02期

关键词：

Sodium selenite; Apoptosis; ER stress; GADD153; ROS; UNFOLDED PROTEIN RESPONSE; OXIDATIVE STRESS; ER STRESS; INVOLVEMENT; SURVIVAL; SIGNALS; ALPHA; UPR;

D O I：

10.1007/s10495-008-0295-5

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In this study, we delineated the apoptotic signaling pathways activated by sodium selenite in NB4 cells. NB4 cells were treated with 20 mu M sodium selenite for different times. The activation of caspases and ER stress markers, ROS levels, mitochondrial membrane potential and cell apoptosis induced by sodium selenite were analyzed by immunoblotting analysis, DCF fluorescence and flow cytometric respectively. siRNA was used to detect the effect of GADD153 on selenite-induced cell apoptosis. Sodium selenite-induced reactive oxygen species generation is an early event that triggers endoplasmic reticulum stress mitochondrial apoptotic pathways in NB4 cells.

引用

页码：218 / 225

页数：8

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