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Article: Transgenic cyclooxygenase-2 expression and high salt enhanced susceptibility to chemical-induced gastric cancer development in mice

TitleTransgenic cyclooxygenase-2 expression and high salt enhanced susceptibility to chemical-induced gastric cancer development in mice
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2008
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2008, v. 29 n. 8, p. 1648-1654 How to Cite?
AbstractCyclooxoygenase (COX)-2 overexpression is involved in gastric carcinogenesis. While high-salt intake is a known risk factor for gastric cancer development, we determined the effects of high salt on gastric chemical carcinogenesis in COX-2 transgenic (TG) mice. COX-2 TG mice were developed in C57/BL6 strain using the full-length human cox-2 complementary DNA construct. Six-week-old COX-2 TG and wild-type (WT) littermates were randomly allocated to receive alternate week of N-methyl-N-nitrosourea (MNU, 240 p.p.m.) in drinking water or control for 10 weeks. Two groups of mice were further treated with 10% NaCl during the initial 10 weeks. All mice were killed at the end of week 50. Both forced COX-2 overexpression and high-salt intake significantly increased the frequency of gastric cancer development in mice as compared with WT littermates treated with MNU alone. However, no additive effect was observed on the combination of high salt and COX-2 expression. We further showed that MNU and high-salt treatment increased chronic inflammatory infiltrates and induced prostaglandin E2 (PGE2) production in the non-cancerous stomach. Whereas high-salt treatment markedly increased the expression of inflammatory cytokines (tumor necrosis factor-α, interferon-γ, interleukin (IL)-1β and IL-6) in the gastric mucosa, COX-2 overexpression significantly altered the cell kinetics in the MNU-induced gastric cancer model. In conclusion, both high salt and COX-2 overexpression promote chemical-induced gastric carcinogenesis, possibly related to chronic inflammation, induction of PGE2, disruption of cell kinetics and induction of inflammatory cytokines. © The Author 2008. Published by Oxford University Press. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/132850
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLeung, WKen_HK
dc.contributor.authorWu, KCen_HK
dc.contributor.authorWong, CYPen_HK
dc.contributor.authorCheng, ASLen_HK
dc.contributor.authorChing, AKKen_HK
dc.contributor.authorChan, AWHen_HK
dc.contributor.authorChong, WWSen_HK
dc.contributor.authorGo, MYYen_HK
dc.contributor.authorYu, Jen_HK
dc.contributor.authorTo, KFen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorChui, Ylen_HK
dc.contributor.authorFan, DMen_HK
dc.contributor.authorSung, JJYen_HK
dc.date.accessioned2011-04-04T07:57:25Z-
dc.date.available2011-04-04T07:57:25Z-
dc.date.issued2008en_HK
dc.identifier.citationCarcinogenesis, 2008, v. 29 n. 8, p. 1648-1654en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/132850-
dc.description.abstractCyclooxoygenase (COX)-2 overexpression is involved in gastric carcinogenesis. While high-salt intake is a known risk factor for gastric cancer development, we determined the effects of high salt on gastric chemical carcinogenesis in COX-2 transgenic (TG) mice. COX-2 TG mice were developed in C57/BL6 strain using the full-length human cox-2 complementary DNA construct. Six-week-old COX-2 TG and wild-type (WT) littermates were randomly allocated to receive alternate week of N-methyl-N-nitrosourea (MNU, 240 p.p.m.) in drinking water or control for 10 weeks. Two groups of mice were further treated with 10% NaCl during the initial 10 weeks. All mice were killed at the end of week 50. Both forced COX-2 overexpression and high-salt intake significantly increased the frequency of gastric cancer development in mice as compared with WT littermates treated with MNU alone. However, no additive effect was observed on the combination of high salt and COX-2 expression. We further showed that MNU and high-salt treatment increased chronic inflammatory infiltrates and induced prostaglandin E2 (PGE2) production in the non-cancerous stomach. Whereas high-salt treatment markedly increased the expression of inflammatory cytokines (tumor necrosis factor-α, interferon-γ, interleukin (IL)-1β and IL-6) in the gastric mucosa, COX-2 overexpression significantly altered the cell kinetics in the MNU-induced gastric cancer model. In conclusion, both high salt and COX-2 overexpression promote chemical-induced gastric carcinogenesis, possibly related to chronic inflammation, induction of PGE2, disruption of cell kinetics and induction of inflammatory cytokines. © The Author 2008. Published by Oxford University Press. All rights reserved.en_HK
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.subjectChemicals And Cas Registry Numbersen_US
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshCell Divisionen_HK
dc.subject.meshCyclooxygenase 2 - geneticsen_HK
dc.subject.meshDNA - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGenetic Predisposition to Diseaseen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMethylnitrosourea - toxicityen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshOviducts - enzymologyen_HK
dc.subject.meshPseudopregnancy - enzymologyen_HK
dc.subject.meshSodium Chloride, Dietary - toxicityen_HK
dc.subject.meshStomach Neoplasms - chemically induced - enzymology - genetics - pathologyen_HK
dc.titleTransgenic cyclooxygenase-2 expression and high salt enhanced susceptibility to chemical-induced gastric cancer development in miceen_HK
dc.typeArticleen_HK
dc.identifier.emailLeung, WK:waikleung@hku.hken_HK
dc.identifier.authorityLeung, WK=rp01479en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1093/carcin/bgn156en_HK
dc.identifier.pmid18611916en_HK
dc.identifier.scopuseid_2-s2.0-49649116457en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-49649116457&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume29en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1648en_HK
dc.identifier.epage1654en_HK
dc.identifier.eissn1460-2180-
dc.identifier.isiWOS:000258471900024-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLeung, WK=7201504523en_HK
dc.identifier.scopusauthoridWu, KC=8947728400en_HK
dc.identifier.scopusauthoridWong, CYP=25947838400en_HK
dc.identifier.scopusauthoridCheng, ASL=7402075036en_HK
dc.identifier.scopusauthoridChing, AKK=35083263600en_HK
dc.identifier.scopusauthoridChan, AWH=25930306100en_HK
dc.identifier.scopusauthoridChong, WWS=24576241300en_HK
dc.identifier.scopusauthoridGo, MYY=7101882939en_HK
dc.identifier.scopusauthoridYu, J=35351306800en_HK
dc.identifier.scopusauthoridTo, KF=7101911940en_HK
dc.identifier.scopusauthoridWang, X=35235704600en_HK
dc.identifier.scopusauthoridChui, Yl=7004982375en_HK
dc.identifier.scopusauthoridFan, DM=7202965595en_HK
dc.identifier.scopusauthoridSung, JJY=35405352400en_HK

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