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Article: XAF1 mediates apoptosis through an extracellular signal-regulated kinase pathway in colon cancer

TitleXAF1 mediates apoptosis through an extracellular signal-regulated kinase pathway in colon cancer
Authors
KeywordsExtracellular signal-regulated kinase
Inhibitors of apoptosis proteins
X chromosome-linked IAP
XIAP-associated factor 1
Issue Date2007
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741
Citation
Cancer, 2007, v. 109 n. 10, p. 1996-2003 How to Cite?
AbstractBACKGROUND. XIAP-associated factor 1 (XAF1) negatively regulates the function of the X-linked inhibitor of apoptosis protein (XIAP), a member of the IAP family that exerts antiapoptotic effects. The extracellular signal-regulated kinase (ERK) pathway is thought to increase cell proliferation and to protect cells from apoptosis. The aim of the study was to investigate the correlation between the ERK1/ 2 signaling pathway and XAF1 in colon cancer. METHODS. Four human colon cancer cell lines, HCT1116 and Lovo (wildtype p53), DLD1 and SW1116 (mutant p53), were used. Lovo stable transfectants with XAF1 sense and antisense were established. The effects of dominant-negative MEK1 (DN-MEK1) and MEK-speciflc inhibitor U0126 on the ERK signaling pathway and expression of XAF1 and XIAP proteins were determined. The transcription activity of core XAF1 promoter was assessed by dual luciferase reporter assay. Cell proliferation was measured by MTT assay. Apoptosis was determined by Hoechst 33258 staining. RESULTS. U0126 increased the expression of XAF1 in a time- and dose-dependent manner. A similar result was obtained in cells transfected with DN-MEK1 treatment. Conversely, the expression of XIAP was down-regulated. Activity of the putative promoter of the XAF1 gene was significantly increased by U0126 treatment and DN-MEK1 transient transfection. rhEGF-stimulated phosphorylation of ERK appeared to have little or no effect on XAF1 expression. Overexpression of XAF1 was more sensitive to U0126-induced apoptosis, whereas down-regulation of XAF1 by antisense reversed U0126-induced inhibition of cell proliferation. CONCLUSIONS. XAF1 expression was up-regulated by inhibition of the ERK1/2 pathway through transcriptional regulation, which required de novo protein synthesis. The results suggest that XAF1 mediates apoptosis induced by the ERK1/2 pathway in colon cancer. © 2007 American Cancer Society.
Persistent Identifierhttp://hdl.handle.net/10722/70158
ISSN
2015 Impact Factor: 5.649
2015 SCImago Journal Rankings: 3.188
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLi, FYen_HK
dc.contributor.authorWang, Jen_HK
dc.contributor.authorZou, Ben_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorYun, LWen_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorYun, WSen_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorHe, Hen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorHsiang, FKen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-06T06:20:16Z-
dc.date.available2010-09-06T06:20:16Z-
dc.date.issued2007en_HK
dc.identifier.citationCancer, 2007, v. 109 n. 10, p. 1996-2003en_HK
dc.identifier.issn0008-543Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/70158-
dc.description.abstractBACKGROUND. XIAP-associated factor 1 (XAF1) negatively regulates the function of the X-linked inhibitor of apoptosis protein (XIAP), a member of the IAP family that exerts antiapoptotic effects. The extracellular signal-regulated kinase (ERK) pathway is thought to increase cell proliferation and to protect cells from apoptosis. The aim of the study was to investigate the correlation between the ERK1/ 2 signaling pathway and XAF1 in colon cancer. METHODS. Four human colon cancer cell lines, HCT1116 and Lovo (wildtype p53), DLD1 and SW1116 (mutant p53), were used. Lovo stable transfectants with XAF1 sense and antisense were established. The effects of dominant-negative MEK1 (DN-MEK1) and MEK-speciflc inhibitor U0126 on the ERK signaling pathway and expression of XAF1 and XIAP proteins were determined. The transcription activity of core XAF1 promoter was assessed by dual luciferase reporter assay. Cell proliferation was measured by MTT assay. Apoptosis was determined by Hoechst 33258 staining. RESULTS. U0126 increased the expression of XAF1 in a time- and dose-dependent manner. A similar result was obtained in cells transfected with DN-MEK1 treatment. Conversely, the expression of XIAP was down-regulated. Activity of the putative promoter of the XAF1 gene was significantly increased by U0126 treatment and DN-MEK1 transient transfection. rhEGF-stimulated phosphorylation of ERK appeared to have little or no effect on XAF1 expression. Overexpression of XAF1 was more sensitive to U0126-induced apoptosis, whereas down-regulation of XAF1 by antisense reversed U0126-induced inhibition of cell proliferation. CONCLUSIONS. XAF1 expression was up-regulated by inhibition of the ERK1/2 pathway through transcriptional regulation, which required de novo protein synthesis. The results suggest that XAF1 mediates apoptosis induced by the ERK1/2 pathway in colon cancer. © 2007 American Cancer Society.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741en_HK
dc.relation.ispartofCanceren_HK
dc.rightsCancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectExtracellular signal-regulated kinaseen_HK
dc.subjectInhibitors of apoptosis proteinsen_HK
dc.subjectX chromosome-linked IAPen_HK
dc.subjectXIAP-associated factor 1en_HK
dc.subject.meshApoptosis - drug effects - physiologyen_HK
dc.subject.meshButadienes - pharmacologyen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshColonic Neoplasms - metabolismen_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshEnzyme Inhibitors - pharmacologyen_HK
dc.subject.meshEpidermal Growth Factor - pharmacologyen_HK
dc.subject.meshExtracellular Signal-Regulated MAP Kinases - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntracellular Signaling Peptides and Proteinsen_HK
dc.subject.meshMAP Kinase Kinase 1 - antagonists & inhibitors - metabolismen_HK
dc.subject.meshMitogen-Activated Protein Kinase 1en_HK
dc.subject.meshNeoplasm Proteins - metabolismen_HK
dc.subject.meshNitriles - pharmacologyen_HK
dc.subject.meshPhosphorylationen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshTranscriptional Activationen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshUp-Regulationen_HK
dc.subject.meshX-Linked Inhibitor of Apoptosis Protein - genetics - metabolismen_HK
dc.titleXAF1 mediates apoptosis through an extracellular signal-regulated kinase pathway in colon canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-543X&volume=109&issue=10&spage=1996&epage=2003&date=2007&atitle=XAF1+Mediates+Apoptosis+Through+an+Extracellular+Signal-Regulated+Kinase+Pathway+in+Colon+Cancer+en_HK
dc.identifier.emailWang, J: jidewang@gmail.comen_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityWang, J=rp00491en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/cncr.22624en_HK
dc.identifier.pmid17385215en_HK
dc.identifier.scopuseid_2-s2.0-34248335752en_HK
dc.identifier.hkuros142121en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34248335752&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume109en_HK
dc.identifier.issue10en_HK
dc.identifier.spage1996en_HK
dc.identifier.epage2003en_HK
dc.identifier.isiWOS:000246252800010-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLi, FY=35313959800en_HK
dc.identifier.scopusauthoridWang, J=35309087500en_HK
dc.identifier.scopusauthoridZou, B=35228257300en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridYun, LW=35314192400en_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridYun, WS=16205603300en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridHe, H=36185495900en_HK
dc.identifier.scopusauthoridLam, SK=7402279800en_HK
dc.identifier.scopusauthoridHsiang, FK=16306692200en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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