Mitogen-activated Protein Kinase Inhibitors Induce Apoptosis and Enhance the Diallyl Disulfide-induced Apoptotic Effect in Human CNE2 Cells

Jun Wen; Xiao Chun Wang; Yi Wei Zhang; Ya Li Nie; Simon G. Talbot; Gloria C. Li; Jian Bo Xiao; Ming Xu

doi:10.1248/jhs.54.129

REGULAR ARTICLES

Mitogen-activated Protein Kinase Inhibitors Induce Apoptosis and Enhance the Diallyl Disulfide-induced Apoptotic Effect in Human CNE2 Cells

Jun Wen, Xiao Chun Wang, Yi Wei Zhang, Ya Li Nie, Simon G. Talbot, Gloria C. Li, Jian Bo Xiao, Ming Xu

Author information

Jun Wen
Research Institute for Molecular Pharmacology and Therapeutics, Central South University
Xiao Chun Wang
Department of Medical Laboratories, Xiangya Medical College of Central-South University
Yi Wei Zhang
Research Institute for Molecular Pharmacology and Therapeutics, Central South University
Ya Li Nie
Research Institute for Molecular Pharmacology and Therapeutics, Central South University
Simon G. Talbot
Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center
Gloria C. Li
Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center
Jian Bo Xiao
Research Institute for Molecular Pharmacology and Therapeutics, Central South University
Ming Xu
Research Institute for Molecular Pharmacology and Therapeutics, Central South University
Department of Radiation Oncology, Memorial Sloan-Kettering Cancer Center

Keywords: apoptosis, combined effect, CNE2 cell, mitogen-activated protein kinase inhibitor, phosphorylation

JOURNAL FREE ACCESS

2008 Volume 54 Issue 2 Pages 129-136

DOI https://doi.org/10.1248/jhs.54.129

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Abstract

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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