Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to cirsimaritin-induced apoptosis in human gallbladder carcinoma GBC-SD cells
Reactive oxygen species-mediated endoplasmic reticulum stress and mitochondrial dysfunction contribute to cirsimaritin-induced apoptosis in human gallbladder carcinoma GBC-SD cells
复制标题
活性氧介导的内质网应激和线粒体功能障碍导致西西马汀诱导人胆囊癌 GBC-SD 细胞凋亡
DOI：
10.1016/j.canlet.2010.03.008
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发表时间：
2010-09-28
期刊：
影响因子：
9.7
通讯作者：
Liu, Yingbin
中科院分区：
文献类型：
--
作者：
Quan, Zhiwei;Gu, Jun;Liu, Yingbin
本研究旨在探讨天然黄酮类化合物-蓟素对人胆囊癌细胞株GBC-SD的抗肿瘤作用及其机制。Cirsimaritin可抑制GBC-SD细胞的生长并诱导其线粒体凋亡。此外，cirsimaritin触发内质网（ER）应激和下调Akt的磷酸化，而敲低CHOP显着废除Akt的失活和逆转cirsimaritin的促凋亡作用。此外，cirsimaritin引起GBC-SD细胞中活性氧的产生，而抗氧化剂N-乙酰半胱氨酸几乎完全阻断了ER应激和凋亡的激活，表明cirsimaritin诱导的活性氧是触发GBC-SD细胞中ER应激线粒体凋亡途径的早期事件。(C)2010爱思唯尔爱尔兰有限公司版权所有。
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.