File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Cigarette smoke exposure increases ulcerative colitis-associated colonic adenoma formation in mice

TitleCigarette smoke exposure increases ulcerative colitis-associated colonic adenoma formation in mice
Authors
Issue Date2003
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2003, v. 24 n. 8, p. 1407-1413 How to Cite?
AbstractBoth chronic ulcerative colitis and smoking are associated with colorectal cancer in humans. In the present study, we investigated the effects of cigarette smoke (CS) exposure on inflammation-associated tumorigenesis in the mouse colon. Male balb/c mice were allocated into six groups: control, CS (2%), CS (4%), colitis, colitis + CS (2%) and colitis + CS (4%). They were given water or 3% dextran sulfate sodium (DSS) in drinking water for 7 days to induce colitis, with or without 1 h daily exposure to 2 or 4% CS. They were then allowed to drink water for 14 days. The cycle of 7 day DSS ± CS/14 day H2O treatments were repeated twice. Mice were killed immediately or 1 month after the three cycles of treatments. Results indicated colonic adenoma was only found in the colitis group (one out of 11), Colitis + CS (2%) group (seven out of 12) and colitis + CS (4%) group (four out of five) 1 month after three cycles of DSS and/or CS treatment. CS exposure dose-dependently increased adenoma formation in mice with inflamed mucosa. CS exposure plus colitis was strongly associated with a high incidence of dysplasia (P < 0.01) and adenocarcinoma formation (P < 0.01) compared with induction of colitis alone. Colitis induced cell proliferation and apoptosis in colonic tissues. Cigarette smoking significantly attenuated the apoptotic effect by DSS probably via the induction of anti-apoptotic protein bcl-2. The ratio of apoptosis over proliferation was also significantly lower in the colitis + CS groups. Vascular endothelial growth factor and angiogenesis in the colon were also increased by cigarette smoking in animals with colitis. In conclusion, CS promotes inflammation-associated adenoma/adenocarcinoma formation in the mouse colon in a dose-dependent manner. This tumor development is associated with the inhibition of cellular apoptosis and supported by increased angiogenesis.
Persistent Identifierhttp://hdl.handle.net/10722/76585
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, ESLen_HK
dc.contributor.authorYe, YNen_HK
dc.contributor.authorShin, VYen_HK
dc.contributor.authorYuen, STen_HK
dc.contributor.authorLeung, SYen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T07:22:48Z-
dc.date.available2010-09-06T07:22:48Z-
dc.date.issued2003en_HK
dc.identifier.citationCarcinogenesis, 2003, v. 24 n. 8, p. 1407-1413en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76585-
dc.description.abstractBoth chronic ulcerative colitis and smoking are associated with colorectal cancer in humans. In the present study, we investigated the effects of cigarette smoke (CS) exposure on inflammation-associated tumorigenesis in the mouse colon. Male balb/c mice were allocated into six groups: control, CS (2%), CS (4%), colitis, colitis + CS (2%) and colitis + CS (4%). They were given water or 3% dextran sulfate sodium (DSS) in drinking water for 7 days to induce colitis, with or without 1 h daily exposure to 2 or 4% CS. They were then allowed to drink water for 14 days. The cycle of 7 day DSS ± CS/14 day H2O treatments were repeated twice. Mice were killed immediately or 1 month after the three cycles of treatments. Results indicated colonic adenoma was only found in the colitis group (one out of 11), Colitis + CS (2%) group (seven out of 12) and colitis + CS (4%) group (four out of five) 1 month after three cycles of DSS and/or CS treatment. CS exposure dose-dependently increased adenoma formation in mice with inflamed mucosa. CS exposure plus colitis was strongly associated with a high incidence of dysplasia (P < 0.01) and adenocarcinoma formation (P < 0.01) compared with induction of colitis alone. Colitis induced cell proliferation and apoptosis in colonic tissues. Cigarette smoking significantly attenuated the apoptotic effect by DSS probably via the induction of anti-apoptotic protein bcl-2. The ratio of apoptosis over proliferation was also significantly lower in the colitis + CS groups. Vascular endothelial growth factor and angiogenesis in the colon were also increased by cigarette smoking in animals with colitis. In conclusion, CS promotes inflammation-associated adenoma/adenocarcinoma formation in the mouse colon in a dose-dependent manner. This tumor development is associated with the inhibition of cellular apoptosis and supported by increased angiogenesis.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis. Copyright © Oxford University Press.en_HK
dc.subject.meshAdenoma - etiology - pathologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshCell Transformation, Neoplasticen_HK
dc.subject.meshChronic Diseaseen_HK
dc.subject.meshColitis, Ulcerative - etiology - pathologyen_HK
dc.subject.meshColonic Neoplasms - etiology - pathologyen_HK
dc.subject.meshDextran Sulfate - toxicityen_HK
dc.subject.meshEndothelial Growth Factors - metabolismen_HK
dc.subject.meshIntercellular Signaling Peptides and Proteins - metabolismen_HK
dc.subject.meshLymphokines - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshNeovascularization, Pathologic - etiologyen_HK
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - metabolismen_HK
dc.subject.meshSmoking - adverse effectsen_HK
dc.subject.meshVascular Endothelial Growth Factor Aen_HK
dc.subject.meshVascular Endothelial Growth Factorsen_HK
dc.titleCigarette smoke exposure increases ulcerative colitis-associated colonic adenoma formation in miceen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=24&issue=8&spage=1407&epage=1413&date=2003&atitle=Cigarette+smoke+exposure+increases+ulcerative+colitis-associated+colonic+adenoma+formation+in+miceen_HK
dc.identifier.emailLeung, SY:suetyi@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityLeung, SY=rp00359en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/carcin/bgg094en_HK
dc.identifier.pmid12807736-
dc.identifier.scopuseid_2-s2.0-0041887073en_HK
dc.identifier.hkuros80430en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0041887073&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume24en_HK
dc.identifier.issue8en_HK
dc.identifier.spage1407en_HK
dc.identifier.epage1413en_HK
dc.identifier.isiWOS:000184675400013-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridLiu, ESL=7202240071en_HK
dc.identifier.scopusauthoridYe, YN=7401627402en_HK
dc.identifier.scopusauthoridShin, VY=7003491170en_HK
dc.identifier.scopusauthoridYuen, ST=7103160927en_HK
dc.identifier.scopusauthoridLeung, SY=7202044886en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridCho, CH=7403100461en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats