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Article: A mechanistic study of cigarette smoke and cyclooxygenase-2 on proliferation of gastric cancer cells

TitleA mechanistic study of cigarette smoke and cyclooxygenase-2 on proliferation of gastric cancer cells
Authors
Keywordsc-myc
Cigarette smoke
Cyclooxygenase-2
Gastric cancer
Ornithine decarboxylase
Issue Date2004
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taap
Citation
Toxicology And Applied Pharmacology, 2004, v. 195 n. 1, p. 103-112 How to Cite?
AbstractCigarette smoke has been shown to cause gastric cancer. Overexpression of cyclooxygenase-2 (COX-2) is a common characteristic in gastric malignancy. The present study aimed to explore the correlation between cigarette smoke and COX-2 in the promotion of tumorigenesis in human gastric cancer cells (AGS). We further studied the action of COX-2 on other proto-oncogenes on gastric tumor growth. Results showed that chloroform extract (CE) and ethanol extract (EE) from cigarette smoke dose-dependently stimulated gastric cancer cell proliferation, which was accompanied with an activation of ornithine decarboxylase (ODC) activity, COX-2, and c-myc expressions. Both antisense of c-myc and α-difluoromethylornithine (DFMO, specific ODC inhibitor) inhibited cell proliferation without affecting COX-2 expression in response to cigarette smoke extracts (CSE). However, selective COX-2 inhibitor (SC-236) not only blocked the proliferative activity but also the ODC activity and c-myc protein expression by CSE in gastric cancer cells. Further, supplementation of exogenous prostaglandin (PG) E2 reversed all the inhibitory actions of SC-236. Our results underline the importance of COX-2 in the cancer-promoting effect of CSE and its modulation on its downstream growth-related genes, such as c-myc and ODC in cancer cell proliferation. These results reveal that CSE-induced gastric carcinogenesis is via the COX-2/c-myc/ODC and PGE2-dependent pathway. Hence, selective COX-2 inhibitor could be an effective therapeutic agent for gastric cancer in smokers. © 2003 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/83359
ISSN
2015 Impact Factor: 3.847
2015 SCImago Journal Rankings: 1.593
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShin, VYen_HK
dc.contributor.authorLiu, ESLen_HK
dc.contributor.authorYe, YNen_HK
dc.contributor.authorKoo, MWLen_HK
dc.contributor.authorChu, KMen_HK
dc.contributor.authorCho, CHen_HK
dc.date.accessioned2010-09-06T08:40:05Z-
dc.date.available2010-09-06T08:40:05Z-
dc.date.issued2004en_HK
dc.identifier.citationToxicology And Applied Pharmacology, 2004, v. 195 n. 1, p. 103-112en_HK
dc.identifier.issn0041-008Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/83359-
dc.description.abstractCigarette smoke has been shown to cause gastric cancer. Overexpression of cyclooxygenase-2 (COX-2) is a common characteristic in gastric malignancy. The present study aimed to explore the correlation between cigarette smoke and COX-2 in the promotion of tumorigenesis in human gastric cancer cells (AGS). We further studied the action of COX-2 on other proto-oncogenes on gastric tumor growth. Results showed that chloroform extract (CE) and ethanol extract (EE) from cigarette smoke dose-dependently stimulated gastric cancer cell proliferation, which was accompanied with an activation of ornithine decarboxylase (ODC) activity, COX-2, and c-myc expressions. Both antisense of c-myc and α-difluoromethylornithine (DFMO, specific ODC inhibitor) inhibited cell proliferation without affecting COX-2 expression in response to cigarette smoke extracts (CSE). However, selective COX-2 inhibitor (SC-236) not only blocked the proliferative activity but also the ODC activity and c-myc protein expression by CSE in gastric cancer cells. Further, supplementation of exogenous prostaglandin (PG) E2 reversed all the inhibitory actions of SC-236. Our results underline the importance of COX-2 in the cancer-promoting effect of CSE and its modulation on its downstream growth-related genes, such as c-myc and ODC in cancer cell proliferation. These results reveal that CSE-induced gastric carcinogenesis is via the COX-2/c-myc/ODC and PGE2-dependent pathway. Hence, selective COX-2 inhibitor could be an effective therapeutic agent for gastric cancer in smokers. © 2003 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/taapen_HK
dc.relation.ispartofToxicology and Applied Pharmacologyen_HK
dc.subjectc-mycen_HK
dc.subjectCigarette smokeen_HK
dc.subjectCyclooxygenase-2en_HK
dc.subjectGastric canceren_HK
dc.subjectOrnithine decarboxylaseen_HK
dc.titleA mechanistic study of cigarette smoke and cyclooxygenase-2 on proliferation of gastric cancer cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0041-008X&volume=195&issue=1&spage=103&epage=112&date=2004&atitle=A+mechanistic+study+of+cigarette+smoke+and+cyclooxygenase-2+on+proliferation+of+gastric+cancer+cellsen_HK
dc.identifier.emailKoo, MWL: wlkoo@hku.hken_HK
dc.identifier.emailChu, KM: chukm@hkucc.hku.hken_HK
dc.identifier.authorityKoo, MWL=rp00233en_HK
dc.identifier.authorityChu, KM=rp00435en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.taap.2003.10.009en_HK
dc.identifier.pmid14962510-
dc.identifier.scopuseid_2-s2.0-0842281343en_HK
dc.identifier.hkuros85616en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0842281343&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume195en_HK
dc.identifier.issue1en_HK
dc.identifier.spage103en_HK
dc.identifier.epage112en_HK
dc.identifier.isiWOS:000189379400011-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShin, VY=7003491170en_HK
dc.identifier.scopusauthoridLiu, ESL=7202240071en_HK
dc.identifier.scopusauthoridYe, YN=36958724200en_HK
dc.identifier.scopusauthoridKoo, MWL=7004550899en_HK
dc.identifier.scopusauthoridChu, KM=7402453538en_HK
dc.identifier.scopusauthoridCho, CH=7403100461en_HK

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