Induction of ER stress protects gastric cancer cells against apoptosis induced by cisplatin and doxorubicin through activation of p38 MAPK

被引：54

作者：

Feng, Ruo ^{[1
]}

Zhai, Wen Long ^{[2
]}

Yang, Hai Yan ^{[3
]}

Jin, Hui ^{[1
]}

Zhang, Qin Xian ^{[1
]}

机构：

[1] Zhengzhou Univ, Sch Med, Dept Histol & Embryol, Zhengzhou 450001, Henan, Peoples R China

[2] Zhengzhou Univ, Affiliated Hosp 1, Dept Gen Surg, Zhengzhou 450052, Henan, Peoples R China

[3] Zhengzhou Univ, Coll Publ Hlth, Dept Epidemiol, Zhengzhou 450051, Henan, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2011年 / 406卷 / 02期

关键词：

p38; MAPK; ER stress; Gastric cancer; Apopsosis; Cisplatin; Doxorubicin; ENDOPLASMIC-RETICULUM STRESS; CELLULAR-RESPONSE; UP-REGULATION; RESISTANCE; PATHWAY; KINASE; PROLIFERATION; REGULATOR; THERAPY;

D O I：

10.1016/j.bbrc.2011.02.036

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：

We investigated the role of endoplasmic reticulum (ER) stress response and p38 MAPIC pathways in the resistance of gastric cancer cells to chemotherapy. Pretreatment of the gastric cancer cells with the ER stress inducer drastically decreased the apoptotic rate induced by cisplatin or doxorubicin. Induction of ER stress also led to the activation of p38. Inhibition of p38 activity abrogated the effects of ER stress-induced resistance to apoptosis induced by cisplatin- and doxorubicin treatment. Thus, ER-stress response in gastric cancer cells causes resistance to cisplatin- and doxorubicin-induced apoptosis, and ER-stress induced chemo-resistance can be overcome by blocking p38 activity. (C) 2011 Elsevier Inc. All rights reserved.

引用

页码：299 / 304

页数：6

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