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Article: Nicotine promotes colon tumor growth and angiogenesis through β-adrenergic activation

TitleNicotine promotes colon tumor growth and angiogenesis through β-adrenergic activation
Authors
Keywordsβ-adrenoceptors
Colon cancer
Nicotine
Smoking
Issue Date2007
PublisherOxford University Press. The Journal's web site is located at http://toxsci.oxfordjournals.org/
Citation
Toxicological Sciences, 2007, v. 97 n. 2, p. 279-287 How to Cite?
AbstractCigarette smoking is a putative environmental risk factor for colon cancer. Nicotine, an active alkaloid in tobacco, has been implicated in carcinogenesis. In the present study, we demonstrated that oral nicotine administration (50 or 200 μg/ml) for 25 days stimulated growth of human colon cancer xenograft in nude mice. It also increased vascularization in the tumors and elevated cotinine and adrenaline plasma levels. β-Adrenoceptors, cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and vascular endothelial growth factor (VEGF) in tumor tissues were also increased by nicotine. I.p. injection of β1-selective antagonist (atenolol, 5 or 10 mg/kg) or β2-selective antagonist (ICI 118,551, 5, or 10 mg/kg) blocked the nicotine-stimulated tumor growth dose dependently, in which β2-selective antagonist produced a more prominent effect. β-Adrenoceptors blockade also abrogated the stimulatory action of nicotine on microvessel densities as well as cell expression of COX-2, PGE2, and VEGF, in which β2-selective antagonist produced a significant effect. These findings provide a direct evidence that nicotine can enhance colon tumor growth mediated partly by stimulation of β-adrenoceptors, preferentially the β2-adrenoceptors. Activation of β-adrenoceptors and the subsequent stimulation of COX-2, PGE2, and VEGF expression is perhaps an important mechanism in the tumorigenic action of nicotine on colon tumor growth. These data suggest that β-adrenoceptors play a modulatory role in the development of colon cancer and partly elucidate the carcinogenic action of cigarette smoke. © The Author 2007. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/80225
ISSN
2015 Impact Factor: 3.88
2015 SCImago Journal Rankings: 1.686
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, HPSen_HK
dc.contributor.authorYu, Len_HK
dc.contributor.authorLam, EKYen_HK
dc.contributor.authorTai, EKKen_HK
dc.contributor.authorWu, WKKen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T08:03:55Z-
dc.date.available2010-09-06T08:03:55Z-
dc.date.issued2007en_HK
dc.identifier.citationToxicological Sciences, 2007, v. 97 n. 2, p. 279-287en_HK
dc.identifier.issn1096-6080en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80225-
dc.description.abstractCigarette smoking is a putative environmental risk factor for colon cancer. Nicotine, an active alkaloid in tobacco, has been implicated in carcinogenesis. In the present study, we demonstrated that oral nicotine administration (50 or 200 μg/ml) for 25 days stimulated growth of human colon cancer xenograft in nude mice. It also increased vascularization in the tumors and elevated cotinine and adrenaline plasma levels. β-Adrenoceptors, cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and vascular endothelial growth factor (VEGF) in tumor tissues were also increased by nicotine. I.p. injection of β1-selective antagonist (atenolol, 5 or 10 mg/kg) or β2-selective antagonist (ICI 118,551, 5, or 10 mg/kg) blocked the nicotine-stimulated tumor growth dose dependently, in which β2-selective antagonist produced a more prominent effect. β-Adrenoceptors blockade also abrogated the stimulatory action of nicotine on microvessel densities as well as cell expression of COX-2, PGE2, and VEGF, in which β2-selective antagonist produced a significant effect. These findings provide a direct evidence that nicotine can enhance colon tumor growth mediated partly by stimulation of β-adrenoceptors, preferentially the β2-adrenoceptors. Activation of β-adrenoceptors and the subsequent stimulation of COX-2, PGE2, and VEGF expression is perhaps an important mechanism in the tumorigenic action of nicotine on colon tumor growth. These data suggest that β-adrenoceptors play a modulatory role in the development of colon cancer and partly elucidate the carcinogenic action of cigarette smoke. © The Author 2007. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://toxsci.oxfordjournals.org/en_HK
dc.relation.ispartofToxicological Sciencesen_HK
dc.rightsToxicological Sciences. Copyright © Oxford University Press.en_HK
dc.subjectβ-adrenoceptorsen_HK
dc.subjectColon canceren_HK
dc.subjectNicotineen_HK
dc.subjectSmokingen_HK
dc.titleNicotine promotes colon tumor growth and angiogenesis through β-adrenergic activationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1096-6080&volume=97&spage=279&epage=287&date=2007&atitle=Nicotine+promotes+colon+tumor+growth+and+angiogenesis+through+beta-adrenergic+activationen_HK
dc.identifier.emailWong, HPS:hpswong@hkusua.hku.hken_HK
dc.identifier.authorityWong, HPS=rp00808en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/toxsci/kfm060en_HK
dc.identifier.pmid17369603-
dc.identifier.scopuseid_2-s2.0-34447562804en_HK
dc.identifier.hkuros157308en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34447562804&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume97en_HK
dc.identifier.issue2en_HK
dc.identifier.spage279en_HK
dc.identifier.epage287en_HK
dc.identifier.isiWOS:000247178200007-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWong, HPS=8644138100en_HK
dc.identifier.scopusauthoridYu, L=14014378300en_HK
dc.identifier.scopusauthoridLam, EKY=8644138600en_HK
dc.identifier.scopusauthoridTai, EKK=9842278900en_HK
dc.identifier.scopusauthoridWu, WKK=18345422600en_HK
dc.identifier.scopusauthoridCho, CH=14067000400en_HK

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