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Article: Expression of macrophage migration inhibitory factor in esophageal squamous cell carcinoma and effects of bile acids and NSAIDs

TitleExpression of macrophage migration inhibitory factor in esophageal squamous cell carcinoma and effects of bile acids and NSAIDs
Authors
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2005, v. 26 n. 1, p. 11-15 How to Cite?
AbstractThe aim of this study was to determine the macrophage migration inhibitory factor (MIF) protein and mRNA expression in esophageal squamous cell carcinoma (ESCC), and the effect of bile acids, aspirin and a selective cyclooxygenase-2 (COX-2) inhibitor, NS398, on MIF expression in ESCC cells in vitro. Specimens from tumors and the adjacent non-cancerous tissues were obtained from 52 ESCC patients. Western blotting was used for the detection of MIF protein expression, and reverse transcription-polymerase chain reaction (RT-PCR) for MIF mRNA expression. Cells of an ESCC cell line, Eca-109, were treated with chenodeoxycholate (CD, 100 mM), glycochenodeoxycholate (GCD, 1 mM), aspirin (1 mM) or NS398 (1 μM). Enzyme-linked immunosorbent assay (ELISA) and RT-PCR were used to detect the expression of the MIF protein and mRNA, respectively, in the supernatant and cultured cells. Western blotting demonstrated that levels of MIF protein were increased in tumors versus non-malignant tissues, with the expression ratio of MIF over β-actin of 0.93 ± 0.21 and 0.57 ± 0.08, respectively (P=0.012). In vitro, both CD and GCD induced a dramatic increase in MIF protein and mRNA in ESCC cells. On the other hand, aspirin and NS398 significantly decreased MIF protein and mRNA expression, and completely blocked bile acid-induced MIF synthesis in the presence or absence of prostaglandin E2. In conclusion, MIF expression is increased in ESCC. Whereas bile acids induce MIF expression in ESCC cells, aspirin and NS398 significantly inhibit MIF expression, even in the presence of bile acids, via a COX-independent mechanism. © Oxford University Press 2005; all rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/77042
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorZhang, STen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-06T07:27:39Z-
dc.date.available2010-09-06T07:27:39Z-
dc.date.issued2005en_HK
dc.identifier.citationCarcinogenesis, 2005, v. 26 n. 1, p. 11-15en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77042-
dc.description.abstractThe aim of this study was to determine the macrophage migration inhibitory factor (MIF) protein and mRNA expression in esophageal squamous cell carcinoma (ESCC), and the effect of bile acids, aspirin and a selective cyclooxygenase-2 (COX-2) inhibitor, NS398, on MIF expression in ESCC cells in vitro. Specimens from tumors and the adjacent non-cancerous tissues were obtained from 52 ESCC patients. Western blotting was used for the detection of MIF protein expression, and reverse transcription-polymerase chain reaction (RT-PCR) for MIF mRNA expression. Cells of an ESCC cell line, Eca-109, were treated with chenodeoxycholate (CD, 100 mM), glycochenodeoxycholate (GCD, 1 mM), aspirin (1 mM) or NS398 (1 μM). Enzyme-linked immunosorbent assay (ELISA) and RT-PCR were used to detect the expression of the MIF protein and mRNA, respectively, in the supernatant and cultured cells. Western blotting demonstrated that levels of MIF protein were increased in tumors versus non-malignant tissues, with the expression ratio of MIF over β-actin of 0.93 ± 0.21 and 0.57 ± 0.08, respectively (P=0.012). In vitro, both CD and GCD induced a dramatic increase in MIF protein and mRNA in ESCC cells. On the other hand, aspirin and NS398 significantly decreased MIF protein and mRNA expression, and completely blocked bile acid-induced MIF synthesis in the presence or absence of prostaglandin E2. In conclusion, MIF expression is increased in ESCC. Whereas bile acids induce MIF expression in ESCC cells, aspirin and NS398 significantly inhibit MIF expression, even in the presence of bile acids, via a COX-independent mechanism. © Oxford University Press 2005; all rights reserved.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.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshAged, 80 and overen_HK
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - pharmacologyen_HK
dc.subject.meshAspirinen_HK
dc.subject.meshBile Acids and Salts - pharmacologyen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCarcinoma, Squamous Cell - metabolismen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshEnzyme-Linked Immunosorbent Assayen_HK
dc.subject.meshEsophageal Neoplasms - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMacrophage Migration-Inhibitory Factors - biosynthesisen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshRNA, Messenger - analysisen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.titleExpression of macrophage migration inhibitory factor in esophageal squamous cell carcinoma and effects of bile acids and NSAIDsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=26&issue=1&spage=11&epage=15&date=2005&atitle=Expression+of+Macrophage+Migration+Inhibitory+Factor+in+Esophageal+Squamous+Cell+Carcinoma+and+Effects+of+Bile+Acids+and+NSAIDsen_HK
dc.identifier.emailLin, MCM:mcllin@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1093/carcin/bgh279en_HK
dc.identifier.pmid15358635-
dc.identifier.scopuseid_2-s2.0-13444280556en_HK
dc.identifier.hkuros97005en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-13444280556&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume26en_HK
dc.identifier.issue1en_HK
dc.identifier.spage11en_HK
dc.identifier.epage15en_HK
dc.identifier.isiWOS:000226186800002-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridZhang, ST=22935976000en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.citeulike75527-

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