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学科主题: 口腔医学
题名:
Activation of c-Jun N-terminal kinase is required for mevastatin-induced apoptosis of salivary adenoid cystic carcinoma cells
作者: 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
发表日期: 2010-08-01
DOI: 10.1097/CAD.0b013e32833c4b3b
卷: 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
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
项目资助者: Scientific Research Foundation for the Returned Overseas Chinese Scholars, State Education Ministry
WOS记录号: WOS:000279649800003
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/63572
Appears in Collections:北京大学口腔医学院_期刊论文

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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:
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.
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