IR@PKUHSC  > 北京大学口腔医学院
学科主题口腔医学
Activation of c-Jun N-terminal kinase is required for mevastatin-induced apoptosis of salivary adenoid cystic carcinoma cells
Zhang, Shan1,2; Wang, Xiao-Ling3,4; Gan, Ye-Hua1,2; Li, Sheng-Lin1,2
关键词apoptosis cell growth inhibition mitogen-activated protein kinases salivary adenoid cystic carcinoma statin
刊名ANTI-CANCER DRUGS
2010-08-01
DOI10.1097/CAD.0b013e32833c4b3b
21期:7页:678-686
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Pharmacology & Pharmacy
资助者Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry ; Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry
研究领域[WOS]Oncology ; Pharmacology & Pharmacy
关键词[WOS]SMOOTH-MUSCLE-CELLS ; COENZYME-A REDUCTASE ; BREAST-CANCER CELLS ; HMG-COA REDUCTASE ; MAP KINASE ; PROTEIN-KINASES ; GLIOMA-CELLS ; SIMVASTATIN ; LOVASTATIN ; INHIBITION
英文摘要

Statins are inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase, originally developed for lowering cholesterol. Statins also have pleiotropic effects, independent of cholesterol-lowering effects, including induction of apoptosis in various cell lines. However, the mechanism underlying statin-induced apoptosis is still not fully understood. This study aims to explore the proapoptotic effects and underlying mechanisms of statins on human salivary adenoid cystic carcinoma (SACC). Exposure of SACC cells to mevastatin resulted in cell growth inhibition and apoptosis in a dose-dependent manner, accompanied by the release of cytochrome c and cleavage of caspase-3. A remarkable decrease in phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and increase in phosphorylation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated kinase were observed. Furthermore, the JNK-specific inhibitor SP600125, but not the p38-specific inhibitor SB203580, abolished mevastatin-induced cell growth inhibition and apoptosis in SACC cells. This was supported by results in which the JNK inhibitor efficiently blocked mevastatin-induced JNK phosphorylation, but not p38 phosphorylation, and further decreased mevastatin-induced phosphorylation of ERK1/2. Taken together, the results suggest that the JNK pathway was required for mevastatin-induced cell growth inhibition and apoptosis in SACC cells. Statins could be potential anticancer agents for SACC chemotherapy. Anti-Cancer Drugs 21:678-686 (C) 2010 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.

语种英语
所属项目编号2006-331
资助者Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry ; Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry
WOS记录号WOS:000279649800003
Citation statistics
Cited Times:5[WOS]   [WOS Record]     [Related Records in WOS]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/63572
Collection北京大学口腔医学院
作者单位1.Peking Univ, Cent Lab, Sch Stomatol, Beijing 100081, Peoples R China
2.Peking Univ, Cent Lab, Hosp Stomatol, Beijing 100081, Peoples R China
3.Peking Univ, Dept Prevent Dent, Sch Stomatol, Beijing 100081, Peoples R China
4.Peking Univ, Dept Prevent Dent, Hosp Stomatol, Beijing 100081, Peoples R China
Recommended Citation
GB/T 7714
Zhang, Shan,Wang, Xiao-Ling,Gan, Ye-Hua,et al. Activation of c-Jun N-terminal kinase is required for mevastatin-induced apoptosis of salivary adenoid cystic carcinoma cells[J]. ANTI-CANCER DRUGS,2010,21(7):678-686.
APA Zhang, Shan,Wang, Xiao-Ling,Gan, Ye-Hua,&Li, Sheng-Lin.(2010).Activation of c-Jun N-terminal kinase is required for mevastatin-induced apoptosis of salivary adenoid cystic carcinoma cells.ANTI-CANCER DRUGS,21(7),678-686.
MLA Zhang, Shan,et al."Activation of c-Jun N-terminal kinase is required for mevastatin-induced apoptosis of salivary adenoid cystic carcinoma cells".ANTI-CANCER DRUGS 21.7(2010):678-686.
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