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

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

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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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