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Oleanolic acid arrests cell cycle and induces apoptosis via ROS-mediated mitochondrial depolarization and lysosomal membrane permeabilization in human pancreatic cancer cells

文献类型：期刊论文

作者Wei, Jianteng1,3; Liu, Ming1; Liu, Haizhou1; Wang, Hui1,3; Wang, Fengxia4; Zhang, Yuyan5; Han, Lijun1; Lin, Xiukun1,2
刊名JOURNAL OF APPLIED TOXICOLOGY
出版日期2013-08-01
卷号33期号:8页码:756-765
关键词oleanolic acid apoptosis ROS mitochondrial depolarization lysosomal membrane permeabilization
ISSN号0260-437X
通讯作者Lin, XK
中文摘要Oleanolic acid (OA), a pentacyclic triterpenoid, exhibits potential anti-tumor activity against many tumor cell lines. This study aims to examine the anti-tumor activity of OA on pancreatic cancer cells and its potential molecular mechanism. The results showed that the proliferation of Panc-28 cells was inhibited by OA in a concentration-dependent manner, with an IC50 (The half maximal inhibitory concentration) value of 46.35 mu g ml-1, as determined by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. The cell cycle was arrested in S phase and G2/M phase by OA. The study also showed that OA could induce remarkable apoptosis, evidenced by an increased percentage of early/late apoptotic cells, DNA ladder and nuclear morphology change. Further study revealed that OA could induce Reactive Oxygen Species (ROS) generation, mitochondrial depolarization, release of cytochrome C, lysosomal membrane permeabilization and leakage of cathepin B. The expression of apoptosis-correlated proteins was also affected in cells treated with OA, including activation of caspases-3/9 and cleavage of PARP. Further study confirmed that ROS scavenger vitamin C could reverse the apoptosis induced by OA in Panc-28 cells. Our results provide evidence that OA arrests the cell cycle and induces apoptosis, possibly via ROS-mediated mitochondrial and a lysosomal pathway in Panc-28 cells. Copyright (c) 2012 John Wiley & Sons, Ltd.
英文摘要Oleanolic acid (OA), a pentacyclic triterpenoid, exhibits potential anti-tumor activity against many tumor cell lines. This study aims to examine the anti-tumor activity of OA on pancreatic cancer cells and its potential molecular mechanism. The results showed that the proliferation of Panc-28 cells was inhibited by OA in a concentration-dependent manner, with an IC50 (The half maximal inhibitory concentration) value of 46.35 mu g ml-1, as determined by MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay. The cell cycle was arrested in S phase and G2/M phase by OA. The study also showed that OA could induce remarkable apoptosis, evidenced by an increased percentage of early/late apoptotic cells, DNA ladder and nuclear morphology change. Further study revealed that OA could induce Reactive Oxygen Species (ROS) generation, mitochondrial depolarization, release of cytochrome C, lysosomal membrane permeabilization and leakage of cathepin B. The expression of apoptosis-correlated proteins was also affected in cells treated with OA, including activation of caspases-3/9 and cleavage of PARP. Further study confirmed that ROS scavenger vitamin C could reverse the apoptosis induced by OA in Panc-28 cells. Our results provide evidence that OA arrests the cell cycle and induces apoptosis, possibly via ROS-mediated mitochondrial and a lysosomal pathway in Panc-28 cells. Copyright (c) 2012 John Wiley & Sons, Ltd.
WOS标题词Science & Technology ; Life Sciences & Biomedicine
学科主题Toxicology
类目[WOS]Toxicology
研究领域[WOS]Toxicology
关键词[WOS]URSOLIC ACID ; CYTOCHROME-C ; DNA-DAMAGE ; ACTIVATION ; EXPRESSION ; STATISTICS ; INDUCTION ; CLEAVAGE ; GROWTH ; BCL-2
收录类别SCI
原文出处10.1002/jat.2725
语种英语
WOS记录号WOS:000320778400006
公开日期2014-07-17
源URL[http://ir.qdio.ac.cn/handle/337002/16709]  
专题海洋研究所_海洋生物技术研发中心
海洋研究所_实验海洋生物学重点实验室
作者单位1.Chinese Acad Sci, Inst Oceanol, Qingdao 266071, Peoples R China
2.Capital Med Univ, Dept Pharmacol, Beijing 100069, Peoples R China
3.Chinese Acad Sci, Grad Univ, Beijing 100049, Peoples R China
4.Shandong Univ, Sch Pharm, Jinan 250100, Shandong, Peoples R China
5.Qingdao Univ Sci & Technol, Coll Chem Engn, Qingdao 266042, Peoples R China
推荐引用方式
GB/T 7714		 Wei, Jianteng,Liu, Ming,Liu, Haizhou,et al. Oleanolic acid arrests cell cycle and induces apoptosis via ROS-mediated mitochondrial depolarization and lysosomal membrane permeabilization in human pancreatic cancer cells[J]. JOURNAL OF APPLIED TOXICOLOGY,2013,33(8):756-765.
APA Wei, Jianteng.,Liu, Ming.,Liu, Haizhou.,Wang, Hui.,Wang, Fengxia.,...&Lin, Xiukun.(2013).Oleanolic acid arrests cell cycle and induces apoptosis via ROS-mediated mitochondrial depolarization and lysosomal membrane permeabilization in human pancreatic cancer cells.JOURNAL OF APPLIED TOXICOLOGY,33(8),756-765.
MLA Wei, Jianteng,et al."Oleanolic acid arrests cell cycle and induces apoptosis via ROS-mediated mitochondrial depolarization and lysosomal membrane permeabilization in human pancreatic cancer cells".JOURNAL OF APPLIED TOXICOLOGY 33.8(2013):756-765.

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来源：海洋研究所

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