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Article: Regulation of XAF1 expression in human colon cancer cell by interferon β: Activation by the transcription regulator STAT1

TitleRegulation of XAF1 expression in human colon cancer cell by interferon β: Activation by the transcription regulator STAT1
Authors
KeywordsColon cancer
IFNβ
Stat1
XAF1
Issue Date2008
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2008, v. 260 n. 1-2, p. 62-71 How to Cite?
AbstractXIAP-associated factor 1 (XAF1) is a novel tumor suppressor and interferon stimulated gene (ISG). Interferon β (IFNβ) exerts anti-proliferative effect and induces apoptosis through the Jak-Stat signaling cascade by the type I Interferon receptor (IFN-R), which initiates gene transcription of those biological effectors of IFNβ. The aim of this study is to determine the effect of IFNβ on XAF1 expression and the putative mechanisms mediated by the critical role of signal transducers and activators of transcription 1 (Stat1). Gene expression was detected by RT-PCR and Western blot analysis. The promoter activity of XAF1 was examined by luciferase reporter assay. The activity of interferon stimulated response element (ISRE) was assessed by electrophoretic mobility shift assay (EMSA) and quantitative chromatin immunoprecipitation assay (Q-ChIP). Results showed that IFNβ stimulated XAF1 promoter activity in colon cancer cell line DLD1 in a time- and dose-dependent manner. A high affinity ISRE binding element (ISRE-XAF1) was located in -55 to -66 nt upstream of the first ATG site of XAF1 gene. Deletion of ISRE-XAF1 completely abrogated basal and IFNβ-induced promoter activity. IFNβ-induced XAF1 expression was mediated by Stat1 through the interaction with ISRE-XAF1. Knocking down of the Stat1 expression and blocking its phosphorylation decreased IFNβ-induced XAF1 expression. Results suggested that induction of an immediate early response gene-XAF1 by IFNβ was mediated by the transcription regulator Stat1 through the ISRE site within the promoter region of XAF1 gene in colon cancer. © 2007 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/69059
ISSN
2023 Impact Factor: 9.1
2023 SCImago Journal Rankings: 2.595
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorSun, Yen_HK
dc.contributor.authorQiao, Len_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorZou, Ben_HK
dc.contributor.authorYuan, Yen_HK
dc.contributor.authorZhu, Sen_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorCheung, TKen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorChan, AOen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-06T06:10:10Z-
dc.date.available2010-09-06T06:10:10Z-
dc.date.issued2008en_HK
dc.identifier.citationCancer Letters, 2008, v. 260 n. 1-2, p. 62-71en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/69059-
dc.description.abstractXIAP-associated factor 1 (XAF1) is a novel tumor suppressor and interferon stimulated gene (ISG). Interferon β (IFNβ) exerts anti-proliferative effect and induces apoptosis through the Jak-Stat signaling cascade by the type I Interferon receptor (IFN-R), which initiates gene transcription of those biological effectors of IFNβ. The aim of this study is to determine the effect of IFNβ on XAF1 expression and the putative mechanisms mediated by the critical role of signal transducers and activators of transcription 1 (Stat1). Gene expression was detected by RT-PCR and Western blot analysis. The promoter activity of XAF1 was examined by luciferase reporter assay. The activity of interferon stimulated response element (ISRE) was assessed by electrophoretic mobility shift assay (EMSA) and quantitative chromatin immunoprecipitation assay (Q-ChIP). Results showed that IFNβ stimulated XAF1 promoter activity in colon cancer cell line DLD1 in a time- and dose-dependent manner. A high affinity ISRE binding element (ISRE-XAF1) was located in -55 to -66 nt upstream of the first ATG site of XAF1 gene. Deletion of ISRE-XAF1 completely abrogated basal and IFNβ-induced promoter activity. IFNβ-induced XAF1 expression was mediated by Stat1 through the interaction with ISRE-XAF1. Knocking down of the Stat1 expression and blocking its phosphorylation decreased IFNβ-induced XAF1 expression. Results suggested that induction of an immediate early response gene-XAF1 by IFNβ was mediated by the transcription regulator Stat1 through the ISRE site within the promoter region of XAF1 gene in colon cancer. © 2007 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_HK
dc.relation.ispartofCancer Lettersen_HK
dc.rightsCancer Letters. Copyright © Elsevier Ireland Ltd.en_HK
dc.subjectColon canceren_HK
dc.subjectIFNβen_HK
dc.subjectStat1en_HK
dc.subjectXAF1en_HK
dc.subject.meshBase Sequenceen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshColonic Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInterferon Regulatory Factor-1 - metabolismen_HK
dc.subject.meshInterferon-beta - metabolism - pharmacologyen_HK
dc.subject.meshIntracellular Signaling Peptides and Proteinsen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshNeoplasm Proteins - genetics - metabolismen_HK
dc.subject.meshPhosphorylationen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshRNA Interferenceen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshRNA, Small Interfering - metabolismen_HK
dc.subject.meshRecombinant Proteins - metabolismen_HK
dc.subject.meshResponse Elementsen_HK
dc.subject.meshSTAT1 Transcription Factor - metabolismen_HK
dc.subject.meshSignal Transduction - drug effectsen_HK
dc.subject.meshTime Factorsen_HK
dc.subject.meshTranscription, Geneticen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleRegulation of XAF1 expression in human colon cancer cell by interferon β: Activation by the transcription regulator STAT1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3835&volume=260&spage=62&epage=71&date=2008&atitle=Regulation+of+XAF1+Expression+in+Human+Colon+Cancer+Cell+by+Interferon+β:+Activation+by+the+Transcription+Regulator+STAT1en_HK
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.emailYuen, MF: mfyuen@hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2007.10.014en_HK
dc.identifier.pmid18035482-
dc.identifier.scopuseid_2-s2.0-38149058329en_HK
dc.identifier.hkuros139938en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-38149058329&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume260en_HK
dc.identifier.issue1-2en_HK
dc.identifier.spage62en_HK
dc.identifier.epage71en_HK
dc.identifier.isiWOS:000253278400008-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridSun, Y=12776261000en_HK
dc.identifier.scopusauthoridQiao, L=7202151719en_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridZou, B=35228257300en_HK
dc.identifier.scopusauthoridYuan, Y=7402709067en_HK
dc.identifier.scopusauthoridZhu, S=7404391208en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridCheung, TK=7103334158en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridChan, AO=7403167965en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.issnl0304-3835-

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