Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to cirsimaritin-induced apoptosis in human gallbladder carcinoma GBC-SD cells

被引：101

作者：

Quan, Zhiwei ^{[1
]}

Gu, Jun ^{[1
]}

Dong, Ping ^{[1
]}

Lu, Jianhua ^{[1
]}

Wu, Xiangsong ^{[2
]}

Wu, Wenguang ^{[2
]}

Fei, Xiaozhou ^{[2
]}

Li, Songgang ^{[1
]}

Wang, Yong ^{[2
]}

Wang, Jianwei ^{[2
]}

Liu, Yingbin ^{[1
]}

机构：

[1] Shanghai Jiao Tong Univ, Dept Gen Surg, Xinhua Hosp, Affiliated Sch Med, Shanghai 200092, Peoples R China

[2] Zhejiang Univ, Dept Surg, Affiliated Hosp 2, Sch Med, Hangzhou 310009, Zhejiang, Peoples R China

来源：

CANCER LETTERS | 2010年 / 295卷 / 02期

基金：

中国国家自然科学基金;

关键词：

Gallbladder carcinoma; Cirsimaritin; Apoptosis; Reactive oxygen species; Endoplasmic reticulum stress; PROSTATE-CANCER CELLS; CYCLE ARREST; ACTIVATION; PATHWAYS; FLAVONOIDS; ROS; CONSTITUENTS; ANTIOXIDANT; CASPASE; KINASES;

D O I：

10.1016/j.canlet.2010.03.008

中图分类号：

R73 [肿瘤学];

学科分类号：

100214 [肿瘤学];

摘要：

In this study, the anticancer effect of cirsimaritin, a natural flavonoid, against human gallbladder carcinoma cell line GBC-SD and the underlying mechanisms were investigated. Cirsimaritin inhibited the growth of tumor cells and induced mitochondrial apoptosis in GBC-SD cells. In addition, cirsimaritin triggered endoplasmic reticulum (ER) stress and down-regulated the phosphorylation of Akt, while knock-down of CHOP dramatically abrogated the inactivation of Akt and reversed the pro-apoptotic effect of cirsimaritin. Furthermore, cirsimaritin provoked the generation of reactive oxygen species in GBC-SD cells, while the antioxidant N-acetyl cysteine almost completely blocked the activation of ER stress and apoptosis, suggesting cirsimaritin-induced reactive oxygen species is an early event that triggers ER stress mitochondrial apoptotic pathways in GBC-SD cells. (C) 2010 Elsevier Ireland Ltd. All rights reserved.

引用

页码：252 / 259

页数：8

共 40 条

[1]

Garlic compounds generate reactive oxygen species leading to activation of stress kinases and cysteine proteases for apoptosis in human glioblastoma T98G and U87MG cells [J].