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Article: Nicotine promotes cell proliferation via α7-nicotinic acetylcholine receptor and catecholamine-synthesizing enzymes-mediated pathway in human colon adenocarcinoma HT-29 cells

TitleNicotine promotes cell proliferation via α7-nicotinic acetylcholine receptor and catecholamine-synthesizing enzymes-mediated pathway in human colon adenocarcinoma HT-29 cells
Authors
Issue Date2007
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taap
Citation
Toxicology And Applied Pharmacology, 2007, v. 221 n. 3, p. 261-267 How to Cite?
AbstractCigarette smoking has been implicated in colon cancer. Nicotine is a major alkaloid in cigarette smoke. In the present study, we showed that nicotine stimulated HT-29 cell proliferation and adrenaline production in a dose-dependent manner. The stimulatory action of nicotine was reversed by atenolol and ICI 118,551, a β1- and β2-selective antagonist, respectively, suggesting the role of β-adrenoceptors in mediating the action. Nicotine also significantly upregulated the expression of the catecholamine-synthesizing enzymes [tyrosine hydroxylase (TH), dopamine-β-hydroxylase (DβH) and phenylethanolamine N-methyltransferase]. Inhibitor of TH, a rate-limiting enzyme in the catecholamine-biosynthesis pathway, reduced the actions of nicotine on cell proliferation and adrenaline production. Expression of α7-nicotinic acetylcholine receptor (α7-nAChR) was demonstrated in HT-29 cells. Methyllycaconitine, an α7-nAChR antagonist, reversed the stimulatory actions of nicotine on cell proliferation, TH and DβH expression as well as adrenaline production. Taken together, through the action on α7-nAChR nicotine stimulates HT-29 cell proliferation via the upregulation of the catecholamine-synthesis pathway and ultimately adrenaline production and β-adrenergic activation. These data reveal the contributory role α7-nAChR and β-adrenoceptors in the tumorigenesis of colon cancer cells and partly elucidate the carcinogenic action of cigarette smoke on colon cancer. © 2007 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/168115
ISSN
2015 Impact Factor: 3.847
2015 SCImago Journal Rankings: 1.593
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, HPSen_US
dc.contributor.authorYu, Len_US
dc.contributor.authorLam, EKYen_US
dc.contributor.authorTai, EKKen_US
dc.contributor.authorWu, WKKen_US
dc.contributor.authorCho, CHen_US
dc.date.accessioned2012-10-08T03:15:15Z-
dc.date.available2012-10-08T03:15:15Z-
dc.date.issued2007en_US
dc.identifier.citationToxicology And Applied Pharmacology, 2007, v. 221 n. 3, p. 261-267en_US
dc.identifier.issn0041-008Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/168115-
dc.description.abstractCigarette smoking has been implicated in colon cancer. Nicotine is a major alkaloid in cigarette smoke. In the present study, we showed that nicotine stimulated HT-29 cell proliferation and adrenaline production in a dose-dependent manner. The stimulatory action of nicotine was reversed by atenolol and ICI 118,551, a β1- and β2-selective antagonist, respectively, suggesting the role of β-adrenoceptors in mediating the action. Nicotine also significantly upregulated the expression of the catecholamine-synthesizing enzymes [tyrosine hydroxylase (TH), dopamine-β-hydroxylase (DβH) and phenylethanolamine N-methyltransferase]. Inhibitor of TH, a rate-limiting enzyme in the catecholamine-biosynthesis pathway, reduced the actions of nicotine on cell proliferation and adrenaline production. Expression of α7-nicotinic acetylcholine receptor (α7-nAChR) was demonstrated in HT-29 cells. Methyllycaconitine, an α7-nAChR antagonist, reversed the stimulatory actions of nicotine on cell proliferation, TH and DβH expression as well as adrenaline production. Taken together, through the action on α7-nAChR nicotine stimulates HT-29 cell proliferation via the upregulation of the catecholamine-synthesis pathway and ultimately adrenaline production and β-adrenergic activation. These data reveal the contributory role α7-nAChR and β-adrenoceptors in the tumorigenesis of colon cancer cells and partly elucidate the carcinogenic action of cigarette smoke on colon cancer. © 2007 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taapen_US
dc.relation.ispartofToxicology and Applied Pharmacologyen_US
dc.subject.meshAdenocarcinoma - Metabolismen_US
dc.subject.meshAlkaloids - Metabolism - Pharmacologyen_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshColonic Neoplasms - Metabolismen_US
dc.subject.meshDopamine Beta-Hydroxylase - Drug Effects - Metabolismen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEpinephrine - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshNicotine - Metabolism - Pharmacologyen_US
dc.subject.meshNicotinic Agonists - Metabolism - Pharmacologyen_US
dc.subject.meshPhenylethanolamine N-Methyltransferase - Drug Effects - Metabolismen_US
dc.subject.meshReceptors, Adrenergic, Beta - Drug Effects - Physiologyen_US
dc.subject.meshReceptors, Nicotinic - Drug Effects - Metabolismen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshTyrosine 3-Monooxygenase - Drug Effects - Metabolismen_US
dc.subject.meshUp-Regulationen_US
dc.titleNicotine promotes cell proliferation via α7-nicotinic acetylcholine receptor and catecholamine-synthesizing enzymes-mediated pathway in human colon adenocarcinoma HT-29 cellsen_US
dc.typeArticleen_US
dc.identifier.emailWong, HPS:hpswong@hkusua.hku.hken_US
dc.identifier.authorityWong, HPS=rp00808en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.taap.2007.04.002en_US
dc.identifier.pmid17498763-
dc.identifier.scopuseid_2-s2.0-34249776345en_US
dc.identifier.hkuros157304-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34249776345&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume221en_US
dc.identifier.issue3en_US
dc.identifier.spage261en_US
dc.identifier.epage267en_US
dc.identifier.isiWOS:000247278800001-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWong, HPS=8644138100en_US
dc.identifier.scopusauthoridYu, L=16314581700en_US
dc.identifier.scopusauthoridLam, EKY=8644138600en_US
dc.identifier.scopusauthoridTai, EKK=9842278900en_US
dc.identifier.scopusauthoridWu, WKK=8507784700en_US
dc.identifier.scopusauthoridCho, CH=14067000400en_US

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