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

被引：85
|
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 ;
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
收藏
页码：252 / 259
页数：8
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