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Article: c-Jun N-terminal kinase (JNK1) upregulates XIAP-associated factor 1 (XAF1) through interferon regulatory factor 1 (IRF-1) in gastrointestinal cancer

Titlec-Jun N-terminal kinase (JNK1) upregulates XIAP-associated factor 1 (XAF1) through interferon regulatory factor 1 (IRF-1) in gastrointestinal cancer
Authors
Issue Date2009
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2009, v. 30 n. 2, p. 222-229 How to Cite?
AbstractBackground and Aims: X-linked inhibitor of apoptosis protein-associated factor 1 (XAF1) is a tumor suppressor that can sensitize cancer cell to apoptosis. Intrinsic expression of XAF1 in cancer cell is low. Our purpose is to determine the effect of c-Jun N-terminal kinase 1 (JNK1) on XAF1 expression and the putative mechanism. Methods: XAF1 expression in gastrointestinal (GI) cancer cell line AGS and SW1116 was detected by reverse transcription-polymerase chain reaction (PCR), real-time PCR and immunoblotting. The role of JNK1 was assessed by ectopic overexpression with wild-type (JNK1-WT) and dominant-negative (JNK1-DN) JNK1 constructs. The effects of JNK1 activator, interferon (IFN)-α, tumor necrosis factor (TNF)-α and phorbol-12-myristate-13-acetate (PMA), or JNK1 inhibitor, SP600125, were evaluated. An XAF1 promoter reporter pLUC107 with WT or mutated interferon regulatory factor 1-binding element (IRF-E) was used to assess JNK1-induced transcription by dual luciferase assay. Result: Ectopic overexpression of JNK1-WT or treatment with IFN-α, TNF-α and PMA induced whereas SP600125 suppressed intrinsic and induced XAF1 expression. Induction of XAF1 required de novo protein synthesis. Moreover, JNK1 stimulated whereas SP600125 suppressed XAF1 promoter activity. JNK1 stimulated interferon regulatory factor 1 (IRF-1 expression, whereas both IRF-1 small-interfering RNA and site mutation of IRF-E within XAF1 promoter abrogated the effect of JNK1. Conclusion: JNK1 stimulated and mediated the effects of IFN and TNF-α on XAF1 expression through transcriptional regulation by induction of IRF-1. The linkage of JNK1, IRF-1 and XAF1 in the same signal pathway may unravel a novel mechanism in regulation of apoptosis and differentiation of GI cancers. © The Author 2008. Published by Oxford University Press. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/163227
ISSN
2015 Impact Factor: 4.874
2015 SCImago Journal Rankings: 2.439
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Jen_HK
dc.contributor.authorZhang, Wen_HK
dc.contributor.authorZhang, Yen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorZou, Ben_HK
dc.contributor.authorJiang, Ben_HK
dc.contributor.authorPang, Ren_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorQiao, Len_HK
dc.contributor.authorLan, Hen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2012-09-05T05:28:57Z-
dc.date.available2012-09-05T05:28:57Z-
dc.date.issued2009en_HK
dc.identifier.citationCarcinogenesis, 2009, v. 30 n. 2, p. 222-229en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/163227-
dc.description.abstractBackground and Aims: X-linked inhibitor of apoptosis protein-associated factor 1 (XAF1) is a tumor suppressor that can sensitize cancer cell to apoptosis. Intrinsic expression of XAF1 in cancer cell is low. Our purpose is to determine the effect of c-Jun N-terminal kinase 1 (JNK1) on XAF1 expression and the putative mechanism. Methods: XAF1 expression in gastrointestinal (GI) cancer cell line AGS and SW1116 was detected by reverse transcription-polymerase chain reaction (PCR), real-time PCR and immunoblotting. The role of JNK1 was assessed by ectopic overexpression with wild-type (JNK1-WT) and dominant-negative (JNK1-DN) JNK1 constructs. The effects of JNK1 activator, interferon (IFN)-α, tumor necrosis factor (TNF)-α and phorbol-12-myristate-13-acetate (PMA), or JNK1 inhibitor, SP600125, were evaluated. An XAF1 promoter reporter pLUC107 with WT or mutated interferon regulatory factor 1-binding element (IRF-E) was used to assess JNK1-induced transcription by dual luciferase assay. Result: Ectopic overexpression of JNK1-WT or treatment with IFN-α, TNF-α and PMA induced whereas SP600125 suppressed intrinsic and induced XAF1 expression. Induction of XAF1 required de novo protein synthesis. Moreover, JNK1 stimulated whereas SP600125 suppressed XAF1 promoter activity. JNK1 stimulated interferon regulatory factor 1 (IRF-1 expression, whereas both IRF-1 small-interfering RNA and site mutation of IRF-E within XAF1 promoter abrogated the effect of JNK1. Conclusion: JNK1 stimulated and mediated the effects of IFN and TNF-α on XAF1 expression through transcriptional regulation by induction of IRF-1. The linkage of JNK1, IRF-1 and XAF1 in the same signal pathway may unravel a novel mechanism in regulation of apoptosis and differentiation of GI cancers. © 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.subject.meshAnthracenes - Pharmacologyen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshGastrointestinal Neoplasms - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshInterferon Regulatory Factor-1 - Metabolismen_US
dc.subject.meshInterferon-Alpha - Metabolismen_US
dc.subject.meshIntracellular Signaling Peptides And Proteinsen_US
dc.subject.meshMitogen-Activated Protein Kinase 8 - Genetics - Physiologyen_US
dc.subject.meshMutationen_US
dc.subject.meshNeoplasm Proteins - Biosynthesis - Geneticsen_US
dc.subject.meshPhorbol Esters - Pharmacologyen_US
dc.subject.meshPromoter Regions, Geneticen_US
dc.subject.meshTranscriptional Activationen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Pharmacologyen_US
dc.subject.meshUp-Regulationen_US
dc.titlec-Jun N-terminal kinase (JNK1) upregulates XIAP-associated factor 1 (XAF1) through interferon regulatory factor 1 (IRF-1) in gastrointestinal canceren_HK
dc.typeArticleen_HK
dc.identifier.emailWang, J: jidewang@gmail.comen_HK
dc.identifier.emailPang, R: robertap@hku.hken_HK
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityWang, J=rp00491en_HK
dc.identifier.authorityPang, R=rp00274en_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1093/carcin/bgn271en_HK
dc.identifier.pmid19056926-
dc.identifier.scopuseid_2-s2.0-60149110314en_HK
dc.identifier.hkuros155717-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-60149110314&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume30en_HK
dc.identifier.issue2en_HK
dc.identifier.spage222en_HK
dc.identifier.epage229en_HK
dc.identifier.isiWOS:000263162500005-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridWang, J=35309087500en_HK
dc.identifier.scopusauthoridZhang, W=7409428339en_HK
dc.identifier.scopusauthoridZhang, Y=36129128700en_HK
dc.identifier.scopusauthoridChen, Y=7601429966en_HK
dc.identifier.scopusauthoridZou, B=35228257300en_HK
dc.identifier.scopusauthoridJiang, B=34770534200en_HK
dc.identifier.scopusauthoridPang, R=7004376659en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridQiao, L=7202151719en_HK
dc.identifier.scopusauthoridLan, H=24544799000en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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