| Resveratrol induces apoptosis of human nasopharyngeal carcinoma cells via activation of multiple apoptotic pathways. | |
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MedLine Citation:
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PMID: 20717957 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Tsung-Teng Huang; Hung-Chi Lin; Chang-Chieh Chen; Chia-Chen Lu; Chia-Fong Wei; Ting-Shu Wu; Fu-Guo Liu; Hsin-Chih Lai |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of cellular physiology Volume: 226 ISSN: 1097-4652 ISO Abbreviation: J. Cell. Physiol. Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2010-12-30 Completed Date: 2011-01-27 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0050222 Medline TA: J Cell Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 720-8 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Wiley-Liss, Inc. |
Affiliation:
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Department of Life Science, National Central University, and Department of Internal Medicine, Chang Gung Memorial Hospital, Taoyuan, Taiwan, Republic of China. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis
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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:
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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
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