Document Detail


Resveratrol induces apoptosis of human nasopharyngeal carcinoma cells via activation of multiple apoptotic pathways.
MedLine Citation:
PMID:  20717957     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Resveratrol, a naturally occurring dietary compound with chemopreventive properties has been reported to trigger a variety of cancer cell types to apoptosis. Whether resveratrol shows any activity on human nasopharyngeal carcinoma (NPC) cells remained to be determined. The aim of this study was to investigate the effect and mechanism of resveratrol on human NPC cells. Treatment of resveratrol resulted in significant decrease in cell viability of NPC cell lines in a dose- and time-dependent manner. A dose-dependent apoptotic cell death was also measured by flow cytometery analysis. Molecular mechanistic studies of apoptosis unraveled resveratrol treatment resulted in a significant loss of mitochondrial transmembrane potential, release of cytochrome c, enhanced expression of Fas ligand (FasL), and suppression of glucose-regulated protein 78 kDa (GRP78). These were followed by activation of caspases-9, -8, -4, and -3, subsequently leading to DNA fragmentation and cell apoptosis. Furthermore, up-regulation of proapoptotic Bax and down-regulation of antiapoptotic Bcl-2 protein were also observed. Taken together, resveratrol induces apoptosis in human NPC cells through regulation of multiple apoptotic pathways, including death receptor, mitochondria, and endoplasmic reticulum (ER) stress. Resveratrol can be developed as an effective compound for human NPC treatment.
Authors:
Tsung-Teng Huang; Hung-Chi Lin; Chang-Chieh Chen; Chia-Chen Lu; Chia-Fong Wei; Ting-Shu Wu; Fu-Guo Liu; Hsin-Chih Lai
Related Documents :
11688967 - Downregulation of urokinase-type plasminogen activator receptor (upar) induces caspase-...
16533807 - Apoptosis induction by activator protein 2alpha involves transcriptional repression of ...
11296547 - Non-steroidal anti-inflammatory drugs protect against chondrocyte apoptotic death.
11550087 - Hsp70-dnaj chaperone pairs prevent nitric oxide-mediated apoptosis in raw 264.7 macroph...
16709797 - Cutting edge: t cell ig mucin-3 reduces inflammatory heart disease by increasing ctla-4...
18831567 - Unique cellular interaction of silver nanoparticles: size-dependent generation of react...
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of cellular physiology     Volume:  226     ISSN:  1097-4652     ISO Abbreviation:  J. Cell. Physiol.     Publication Date:  2011 Mar 
Date Detail:
Created Date:  2010-12-30     Completed Date:  2011-01-27     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0050222     Medline TA:  J Cell Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  720-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Wiley-Liss, Inc.
Affiliation:
Department of Life Science, National Central University, and Department of Internal Medicine, Chang Gung Memorial Hospital, Taoyuan, Taiwan, Republic of China.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Apoptosis / drug effects*
Caspases / metabolism
Cell Line, Tumor
Cell Survival / drug effects
DNA Fragmentation / drug effects
Drug Screening Assays, Antitumor
Fas Ligand Protein / genetics,  metabolism
Gene Expression Regulation, Neoplastic / drug effects
Heat-Shock Proteins / genetics,  metabolism
Humans
Membrane Potential, Mitochondrial / drug effects
Models, Biological
Nasopharyngeal Neoplasms / enzymology,  genetics,  pathology
Proto-Oncogene Proteins c-bcl-2 / genetics,  metabolism
Signal Transduction / drug effects*
Stilbenes / pharmacology*
Transcription Factor CHOP / genetics,  metabolism
Chemical
Reg. No./Substance:
0/DDIT3 protein, human; 0/Fas Ligand Protein; 0/Heat-Shock Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/Stilbenes; 0/molecular chaperone GRP78; 147336-12-7/Transcription Factor CHOP; 501-36-0/resveratrol; EC 3.4.22.-/Caspases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Rab11b and its effector Rip11 regulate the acidosis-induced traffic of V-ATPase in salivary ducts.
Next Document:  Physiological implications of adenosine receptor-mediated platelet aggregation.