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Article: Nicotine induces cyclooxygenase-2 and vascular endothelial growth factor receptor-2 in association with tumor-associated invasion and angiogenesis in gastric cancer

TitleNicotine induces cyclooxygenase-2 and vascular endothelial growth factor receptor-2 in association with tumor-associated invasion and angiogenesis in gastric cancer
Authors
Issue Date2005
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://mcr.aacrjournals.org/
Citation
Molecular Cancer Research, 2005, v. 3 n. 11, p. 607-615 How to Cite?
AbstractBlockade of angiogenesis is a promising strategy to suppress tumor growth, invasion, and metastasis. Vascular endothelial growth factor (VEGF), which binds to tyrosine kinase receptors [VEGF receptors (VEGFR) 1 and 2], is the mediator of angiogenesis and mitogen for endothelial cells. Cyclooxygenase-2 (COX-2) plays an important role in the promoting action of nicotine on gastric cancer growth. However, the action of nicotine and the relationship between COX-2 and VEGF/VEGFR system in tumorigenesis remain undefined. In this study, the effects of nicotine in tumor angiogenesis, invasiveness, and metastasis were studied with sponge implantation and Matrigel membrane models. Nicotine (200 μg/mL) stimulated gastric cancer cell proliferation, which was blocked by SC-236 (a highly selective COX-2 inhibitor) and CBO-P11 (a VEGFR inhibitor). This was associated with decreased VEGF levels as well as VEGFR-2 but not VEGFR-1 expression. Topical injection of nicotine enhanced tumor-associated vascularization, with a concomitant increase in VEGF levels in sponge implants. Again, application of SC-236 (2 mg/kg) and CBO-P11 (0.4 mg/kg) partially attenuated vascularization by ∼30%. Furthermore, nicotine enhanced tumor cell invasion through the Matrigel membrane by 4-fold and promoted migration of human umbilical vein endothelial cells in a cocultured system with gastric cancer cells. The activity of matrix metalloproteinases 2 and 9 and protein expressions of plasminogen activators (urokinase-type plasminogen activator and its receptor), which are the indicators of invasion and migration processes, were increased by nicotine but blocked by COX-2 and VEGFR inhibitors. Taken together, our results reveal that the promoting action of nicotine on angiogenesis, tumor invasion, and metastasis is COX-2/VEGF/VEGFR dependent. Copyright © 2005 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/80213
ISSN
2015 Impact Factor: 4.51
2015 SCImago Journal Rankings: 2.534
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShin, VYen_HK
dc.contributor.authorWu, WKKen_HK
dc.contributor.authorChu, KMen_HK
dc.contributor.authorWong, HPSen_HK
dc.contributor.authorLam, EKYen_HK
dc.contributor.authorTai, EKKen_HK
dc.contributor.authorKoo, MWLen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T08:03:47Z-
dc.date.available2010-09-06T08:03:47Z-
dc.date.issued2005en_HK
dc.identifier.citationMolecular Cancer Research, 2005, v. 3 n. 11, p. 607-615en_HK
dc.identifier.issn1541-7786en_HK
dc.identifier.urihttp://hdl.handle.net/10722/80213-
dc.description.abstractBlockade of angiogenesis is a promising strategy to suppress tumor growth, invasion, and metastasis. Vascular endothelial growth factor (VEGF), which binds to tyrosine kinase receptors [VEGF receptors (VEGFR) 1 and 2], is the mediator of angiogenesis and mitogen for endothelial cells. Cyclooxygenase-2 (COX-2) plays an important role in the promoting action of nicotine on gastric cancer growth. However, the action of nicotine and the relationship between COX-2 and VEGF/VEGFR system in tumorigenesis remain undefined. In this study, the effects of nicotine in tumor angiogenesis, invasiveness, and metastasis were studied with sponge implantation and Matrigel membrane models. Nicotine (200 μg/mL) stimulated gastric cancer cell proliferation, which was blocked by SC-236 (a highly selective COX-2 inhibitor) and CBO-P11 (a VEGFR inhibitor). This was associated with decreased VEGF levels as well as VEGFR-2 but not VEGFR-1 expression. Topical injection of nicotine enhanced tumor-associated vascularization, with a concomitant increase in VEGF levels in sponge implants. Again, application of SC-236 (2 mg/kg) and CBO-P11 (0.4 mg/kg) partially attenuated vascularization by ∼30%. Furthermore, nicotine enhanced tumor cell invasion through the Matrigel membrane by 4-fold and promoted migration of human umbilical vein endothelial cells in a cocultured system with gastric cancer cells. The activity of matrix metalloproteinases 2 and 9 and protein expressions of plasminogen activators (urokinase-type plasminogen activator and its receptor), which are the indicators of invasion and migration processes, were increased by nicotine but blocked by COX-2 and VEGFR inhibitors. Taken together, our results reveal that the promoting action of nicotine on angiogenesis, tumor invasion, and metastasis is COX-2/VEGF/VEGFR dependent. Copyright © 2005 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://mcr.aacrjournals.org/en_HK
dc.relation.ispartofMolecular Cancer Researchen_HK
dc.titleNicotine induces cyclooxygenase-2 and vascular endothelial growth factor receptor-2 in association with tumor-associated invasion and angiogenesis in gastric canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1541-7786&volume=3&issue=11&spage=607&epage=15&date=2005&atitle=Nicotine+induces+cyclooxygenase-2+and+vascular+endothelial+growth+factor+receptor-2+in+association+with+tumor-associated+invasion+and+angiogenesis+in+gastric+canceren_HK
dc.identifier.emailChu, KM: chukm@hkucc.hku.hken_HK
dc.identifier.emailWong, HPS: hpswong@hkusua.hku.hken_HK
dc.identifier.emailKoo, MWL: wlkoo@hku.hken_HK
dc.identifier.authorityChu, KM=rp00435en_HK
dc.identifier.authorityWong, HPS=rp00808en_HK
dc.identifier.authorityKoo, MWL=rp00233en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1158/1541-7786.MCR-05-0106en_HK
dc.identifier.pmid16317086-
dc.identifier.scopuseid_2-s2.0-28844483289en_HK
dc.identifier.hkuros119221en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-28844483289&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume3en_HK
dc.identifier.issue11en_HK
dc.identifier.spage607en_HK
dc.identifier.epage615en_HK
dc.identifier.isiWOS:000233959900002-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShin, VY=7003491170en_HK
dc.identifier.scopusauthoridWu, WKK=18345422600en_HK
dc.identifier.scopusauthoridChu, KM=7402453538en_HK
dc.identifier.scopusauthoridWong, HPS=8644138100en_HK
dc.identifier.scopusauthoridLam, EKY=8644138600en_HK
dc.identifier.scopusauthoridTai, EKK=9842278900en_HK
dc.identifier.scopusauthoridKoo, MWL=7004550899en_HK
dc.identifier.scopusauthoridCho, CH=7403100461en_HK

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