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Article: Functional role of β-adrenergic receptors in the mitogenic action of nicotine on gastric cancer cells

TitleFunctional role of β-adrenergic receptors in the mitogenic action of nicotine on gastric cancer cells
Authors
Issue Date2007
PublisherOxford University Press. The Journal's web site is located at http://toxsci.oxfordjournals.org/
Citation
Toxicological Sciences, 2007, v. 96 n. 1, p. 21-29 How to Cite?
AbstractWe previously reported that nicotine promoted gastric cancer cell growth via upregulation of cyclooxygenase 2 (COX-2). In the present study, we further investigated whether β-adrenoceptors, protein kinase C (PKC), and extracellular signal-regulated kinase-1/2 (ERK1/2) were involved in the modulation of COX-2 expression and cell proliferation by nicotine in AGS, a human gastric adenocarcinoma cell line. Results showed that nicotine dose dependently increased the phosphorylation of EKR1/2 and the expression of AP-1 subunits c-fos and c-jun. In this connection, the ERK1/2 inhibitor U0126 abrogated the upregulation of AP-1 and COX-2 as well as cell proliferation induced by nicotine. Moreover, nicotine induced the translocation of PKC-βI from cytosol to membrane and increased the total levels of PKC expression. Inhibition of PKC by staurosporine attenuated nicotine-induced ERK1/2 phosphorylation and COX-2 expression. Furthermore, atenolol and ICI 118,551, a β1- and β2-adrenoceptor antagonist, respectively, reversed the stimulatory action of nicotine on the expression of PKC, ERK1/2 phosphorylation, and COX-2 together with cell proliferation. Collectively, these results suggest that nicotine stimulates gastric cancer cell growth through the activation of β-adrenoceptors and the downstream PKC-βI/ERK1/2/COX-2 pathway. © 2007 Oxford University Press.
Persistent Identifierhttp://hdl.handle.net/10722/172937
ISSN
2015 Impact Factor: 3.88
2015 SCImago Journal Rankings: 1.686
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShin, VYen_US
dc.contributor.authorWu, WKKen_US
dc.contributor.authorChu, KMen_US
dc.contributor.authorKoo, MWLen_US
dc.contributor.authorWong, HPSen_US
dc.contributor.authorLam, EKYen_US
dc.contributor.authorTai, EKKen_US
dc.contributor.authorCho, CHen_US
dc.date.accessioned2012-10-30T06:25:55Z-
dc.date.available2012-10-30T06:25:55Z-
dc.date.issued2007en_US
dc.identifier.citationToxicological Sciences, 2007, v. 96 n. 1, p. 21-29en_US
dc.identifier.issn1096-6080en_US
dc.identifier.urihttp://hdl.handle.net/10722/172937-
dc.description.abstractWe previously reported that nicotine promoted gastric cancer cell growth via upregulation of cyclooxygenase 2 (COX-2). In the present study, we further investigated whether β-adrenoceptors, protein kinase C (PKC), and extracellular signal-regulated kinase-1/2 (ERK1/2) were involved in the modulation of COX-2 expression and cell proliferation by nicotine in AGS, a human gastric adenocarcinoma cell line. Results showed that nicotine dose dependently increased the phosphorylation of EKR1/2 and the expression of AP-1 subunits c-fos and c-jun. In this connection, the ERK1/2 inhibitor U0126 abrogated the upregulation of AP-1 and COX-2 as well as cell proliferation induced by nicotine. Moreover, nicotine induced the translocation of PKC-βI from cytosol to membrane and increased the total levels of PKC expression. Inhibition of PKC by staurosporine attenuated nicotine-induced ERK1/2 phosphorylation and COX-2 expression. Furthermore, atenolol and ICI 118,551, a β1- and β2-adrenoceptor antagonist, respectively, reversed the stimulatory action of nicotine on the expression of PKC, ERK1/2 phosphorylation, and COX-2 together with cell proliferation. Collectively, these results suggest that nicotine stimulates gastric cancer cell growth through the activation of β-adrenoceptors and the downstream PKC-βI/ERK1/2/COX-2 pathway. © 2007 Oxford University Press.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://toxsci.oxfordjournals.org/en_US
dc.relation.ispartofToxicological Sciencesen_US
dc.rightsToxicological Sciences. Copyright © Oxford University Press.-
dc.subject.meshAdenocarcinoma - Metabolism - Physiopathologyen_US
dc.subject.meshAdrenergic Beta-Antagonists - Pharmacologyen_US
dc.subject.meshAtenolol - Pharmacologyen_US
dc.subject.meshButadienes - Pharmacologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshCyclooxygenase 2 - Biosynthesisen_US
dc.subject.meshDose-Response Relationship, Drugen_US
dc.subject.meshEnzyme Induction - Drug Effectsen_US
dc.subject.meshExtracellular Signal-Regulated Map Kinases - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshMembrane Proteins - Biosynthesisen_US
dc.subject.meshMitogens - Pharmacologyen_US
dc.subject.meshNicotine - Pharmacologyen_US
dc.subject.meshNitriles - Pharmacologyen_US
dc.subject.meshPhosphorylation - Drug Effectsen_US
dc.subject.meshPropanolamines - Pharmacologyen_US
dc.subject.meshProtein Kinase C - Metabolismen_US
dc.subject.meshProtein Kinase Inhibitors - Pharmacologyen_US
dc.subject.meshProtein Transport - Drug Effectsen_US
dc.subject.meshReceptors, Adrenergic, Beta - Drug Effects - Metabolismen_US
dc.subject.meshSignal Transduction - Drug Effectsen_US
dc.subject.meshStaurosporine - Pharmacologyen_US
dc.subject.meshStomach Neoplasms - Metabolism - Physiopathologyen_US
dc.subject.meshTranscription Factor Ap-1 - Biosynthesisen_US
dc.titleFunctional role of β-adrenergic receptors in the mitogenic action of nicotine on gastric cancer cellsen_US
dc.typeArticleen_US
dc.identifier.emailChu, KM: chukm@hkucc.hku.hken_US
dc.identifier.emailKoo, MWL: wlkoo@hku.hken_US
dc.identifier.emailWong, HPS: hpswong@hkusua.hku.hken_US
dc.identifier.authorityChu, KM=rp00435en_US
dc.identifier.authorityKoo, MWL=rp00233en_US
dc.identifier.authorityWong, HPS=rp00808en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/toxsci/kfl118en_US
dc.identifier.pmid17003101en_US
dc.identifier.scopuseid_2-s2.0-33847316161en_US
dc.identifier.hkuros126167-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33847316161&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume96en_US
dc.identifier.issue1en_US
dc.identifier.spage21en_US
dc.identifier.epage29en_US
dc.identifier.isiWOS:000244262900004-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridShin, VY=7003491170en_US
dc.identifier.scopusauthoridWu, WKK=18345422600en_US
dc.identifier.scopusauthoridChu, KM=7402453538en_US
dc.identifier.scopusauthoridKoo, MWL=7004550899en_US
dc.identifier.scopusauthoridWong, HPS=8644138100en_US
dc.identifier.scopusauthoridLam, EKY=8644138600en_US
dc.identifier.scopusauthoridTai, EKK=9842278900en_US
dc.identifier.scopusauthoridCho, CH=7403100461en_US
dc.identifier.citeulike1130947-

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