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J.Health Sci., 54(2), 129-136, 2008
Mitogen-activated Protein Kinase Inhibitors Induce Apoptosis and Enhance the Diallyl Disulfide-induced Apoptotic Effect in Human CNE2 Cells
Jun Wen,a Xiao Chun Wang,b
Yi Wei Zhang,a Ya Li Nie,a
Simon G. Talbot,c Gloria C. Li,c
Jian Bo Xiao,a and Ming Xu*, a, c
aResearch Institute for Molecular Pharmacology and Therapeutics, Central South University, Xiangya Road 77, Changsha, Hunan 410083, P.R. China,
bDepartment of Medical Laboratories, Xiangya Medical College of Central-South University, Xiangya Road 77, Changsha, Hunan 410083, P.R. China, and
cDepartment of Radiation Oncology, Memorial Sloan-Kettering Cancer Center, 1275 York Ave, New York, NY 10021, U.S.A.
In this study, we investigated whether the inhibition of endogenous phosphorylation of mitogen-activated protein kinase (MAPK) and diallyl disulfide (DADS)-induced phosphorylation of MAPKs with MAPK specific inhibitors, SB203580 and U0126 (for phospho-p38 and phospho-p42/p44, respectively), can induce or enhance apoptosis in human CNE2 nasopharyngeal carcinoma cells. Our data demonstrate that MAPK inhibitors decrease the viability of CNE2 cells, stimulate typical apoptotic morphologic changes, and enhance DADS-induced apoptosis. The present findings indicate that phosphorylation of MAPKs plays an important cytoprotective role in CNE2 cell apoptosis and the DADS-induced apoptotic process.
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