IR@PKUHSC  > 北京大学基础医学院  > 药理学系
学科主题基础医学
Atorvastatin reduces vascular endothelial growth factor (VEGF) expression in human non-small cell lung carcinomas (NSCLCs) via inhibition of reactive oxygen species (ROS) production
Chen, Jie1,2; Liu, Bing3; Yuan, Jiayi1,2; Yang, Jie4; Zhang, Jingjie1,2; An, Yu1,2; Tie, Lu1,2; Pan, Yan1,2; Li, Xuejun1,2
关键词Non-small Cell Lung Cancers Nsclcs Vascular Endothelial Growth Factor Vegf Reactive Oxygen Species Ros Nadph Oxidase Atorvastatin
刊名MOLECULAR ONCOLOGY
2012-02-01
DOI10.1016/j.molonc.2011.11.003
6期:1页:62-72
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology
研究领域[WOS]Oncology
关键词[WOS]NADPH OXIDASE ACTIVITY ; PROSTATE-CANCER CELLS ; OXIDATIVE STRESS ; MATRIX METALLOPROTEINASES ; GLUTATHIONE-PEROXIDASE ; STATIN TREATMENT ; MESSENGER-RNA ; BREAST-CANCER ; UP-REGULATION ; APOPTOSIS
英文摘要

The high metastatic potential of non-small cell lung cancers (NSCLCs) is closely correlated with the elevated expression of vascular endothelial growth factor (VEGF) and resultant tumor angiogenesis. However, no effective strategies against VEGF expression have been available in NSCLCs therapy. This study demonstrated that elevated reactive oxygen species (ROS) levels derived from both mitochondria and NADPH oxidase were required for VEGF expression in NSCLC cells. Atorvastatin administration could significantly inhibit VEGF expression both in vitro and in vivo via inhibition of ROS production. Atorvastatin inhibited ROS generation partly through suppression of Rac1/NADPH oxidase activity. Specifically, atorvastatin could upregulate the activity of glutathione peroxidase (GPx) and catalase, which are responsible for elimination of hydrogen peroxide (H2O2) in the mitochondria and peroxisomes, respectively. Thus, inhibition of ROS production by concomitant suppression of Rac1/NADPH oxidase activity and upregulation of the activity of GPx and catalase contributes critically to atorvastatin-reduced VEGF expression in NSCLCs. Atorvastatin may be a potential alternative against VEGF expression and angiogenesis in NSCLCs therapy. (C) 2011 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

语种英语
WOS记录号WOS:000300967100006
引用统计
被引频次:31[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/52972
专题北京大学基础医学院_药理学系
北京大学医学部管理机构_医学部
北京大学基础医学院
作者单位1.Peking Univ, Inst Syst Biomed, Beijing 100191, Peoples R China
2.Peking Univ, Key Lab Nat & Biomimet Drugs, Dept Pharmacol, Sch Basic Med Sci, Beijing 100191, Peoples R China
3.Guangdong Pharmaceut Univ, Sch Pharm, Dept Pharmacol, Guangzhou 510006, Guangdong, Peoples R China
4.Guangxi Med Univ, Sch Pharm, Dept Pharmacol, Nanning 530021, Peoples R China
推荐引用方式
GB/T 7714
Chen, Jie,Liu, Bing,Yuan, Jiayi,et al. Atorvastatin reduces vascular endothelial growth factor (VEGF) expression in human non-small cell lung carcinomas (NSCLCs) via inhibition of reactive oxygen species (ROS) production[J]. MOLECULAR ONCOLOGY,2012,6(1):62-72.
APA Chen, Jie.,Liu, Bing.,Yuan, Jiayi.,Yang, Jie.,Zhang, Jingjie.,...&Li, Xuejun.(2012).Atorvastatin reduces vascular endothelial growth factor (VEGF) expression in human non-small cell lung carcinomas (NSCLCs) via inhibition of reactive oxygen species (ROS) production.MOLECULAR ONCOLOGY,6(1),62-72.
MLA Chen, Jie,et al."Atorvastatin reduces vascular endothelial growth factor (VEGF) expression in human non-small cell lung carcinomas (NSCLCs) via inhibition of reactive oxygen species (ROS) production".MOLECULAR ONCOLOGY 6.1(2012):62-72.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Chen, Jie]的文章
[Liu, Bing]的文章
[Yuan, Jiayi]的文章
百度学术
百度学术中相似的文章
[Chen, Jie]的文章
[Liu, Bing]的文章
[Yuan, Jiayi]的文章
必应学术
必应学术中相似的文章
[Chen, Jie]的文章
[Liu, Bing]的文章
[Yuan, Jiayi]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。