| Involvement of human heat shock protein 90 alpha in nicotine-induced apoptosis. | |
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MedLine Citation:
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PMID: 12115584 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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There have been conflicting reports of the apoptotic effects of nicotine on human cells and those studies reporting nicotine-induced apoptosis have not unequivocally clarified the molecular mechanisms underlying the effect. However, we found here that human RSa cells, established from embryonic fibroblastic cells doubly infected with Rous sarcoma virus and Simian virus 40, underwent apoptosis when cultured with medium containing 0.06-0.6 microM nicotine. The apoptosis was assessed by cellular DNA fragmentation and caspase-3 protease activation. Viability of RSa cells was reduced by nicotine treatment, as analyzed by MTT assay and the reduction was lessened by combination treatment with a caspase-3 inhibitor, acetyl-L-aspartyl-L-glutamyl-L-valyl-L-aspart-1-al (Ac-DEVD-CHO). Levels of expression of heat shock protein 90 alpha (Hsp90 alpha) were found to be increased 20 min after the nicotine treatment, as analyzed by polymerase chain reaction-based mRNA differential display after Northern blotting analysis of mRNA amounts. Cellular contents of Hsp90 alpha were furthermore increased in the nicotine-treated RSa cells, as quantitated by Western immunoblot analysis. By contrast, in RSa cells treated with nicotine in combination with geldanamycin (GA), an inhibitor of Hsp90 alpha function, DNA fragmentation was not detected and caspase-3 protease activity levels were the same as those of mock-treated cells. Nicotine-induced caspase-3 activation and Hsp90 alpha expression, as well as suppression of the induction by GA, were also observed in a xeroderma pigmentosum patient-derived cell line, XP2OS cells. Thus, it was suggested that nicotine induces apoptosis, possibly via Hsp90 alpha expression, in human cells tested. |
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Authors:
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Yu-Ping Wu; Kazuko Kita; Nobuo Suzuki |
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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: International journal of cancer. Journal international du cancer Volume: 100 ISSN: 0020-7136 ISO Abbreviation: Int. J. Cancer Publication Date: 2002 Jul |
Date Detail:
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Created Date: 2002-07-12 Completed Date: 2002-07-29 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0042124 Medline TA: Int J Cancer Country: United States |
Other Details:
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Languages: eng Pagination: 37-42 Citation Subset: IM |
Copyright Information:
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Copyright 2002 Wiley-Liss, Inc. |
Affiliation:
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Department of Biochemistry, School of Medicine, Chiba University, Chiba City, Chiba, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis
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drug effects* Avian Sarcoma Viruses Benzoquinones Blotting, Northern Blotting, Western Caspase 3 Caspases / antagonists & inhibitors Cell Line Cysteine Proteinase Inhibitors / pharmacology DNA Fragmentation Embryo, Mammalian Enzyme Inhibitors / pharmacology Fibroblasts / virology HSP90 Heat-Shock Proteins / antagonists & inhibitors, genetics, physiology* Humans Lactams, Macrocyclic Nicotine / pharmacology* Oligopeptides / pharmacology Polymerase Chain Reaction Quinones / pharmacology RNA, Messenger / analysis Reverse Transcriptase Polymerase Chain Reaction Simian virus 40 Ultraviolet Rays |
| Chemical | |
Reg. No./Substance:
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0/Benzoquinones; 0/Cysteine Proteinase Inhibitors; 0/Enzyme Inhibitors; 0/HSP90 Heat-Shock Proteins; 0/Lactams, Macrocyclic; 0/Oligopeptides; 0/Quinones; 0/RNA, Messenger; 0/acetyl-aspartyl-glutamyl-valyl-aspartal; 30562-34-6/geldanamycin; 54-11-5/Nicotine; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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