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Article: XIAP-associated factor 1 (XAF1), a novel target of p53, enhances p53-mediated apoptosis via post-translational modification

TitleXIAP-associated factor 1 (XAF1), a novel target of p53, enhances p53-mediated apoptosis via post-translational modification
Authors
KeywordsApoptosis
Colon cancer
Gastric cancer
P53
XAF1
Issue Date2012
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0899-1987/
Citation
Molecular Carcinogenesis, 2012, v. 51 n. 5, p. 422-432 How to Cite?
AbstractThe role of X chromosome-linked inhibitor of apoptosis protein (XIAP)-associated factor 1 (XAF1) in mediating apoptosis has been reported but the underlying mechanism remains unclear. The present study was designed to examine the putative interaction between XAF1 and p53 and the functional importance of this interaction in regulation of apoptosis in human gastric and colon cancer cells. We first identified XAF1 as a novel target gene of p53 by the chromatin immunoprecipitation (CHIP) assay and demonstrated that wild-type p53, but not mutant p53, down-regulated XAF1 at both mRNA and protein levels, which acted mostly under the condition of high expression of XAF1 and was associated with the physical interaction between p53 and the XAF1 promoter. We also found that the over-expression of XAF1 led to activation of wild-type p53 via post-translational modification in cells with or without DNA damage, which resulting in p53 nuclear accumulation and its increased transcriptional activity and enhancing p53-dependent apoptosis. These findings suggest that a potential novel feedback loop exists between XAF1 and wild-type p53. © 2011 Wiley Periodicals, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/137367
ISSN
2014 Impact Factor: 4.808
2014 SCImago Journal Rankings: 1.397
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong KongHKU-200807176136
Science and Technology Programme of Guangzhou, China2008J1-C261-3
Funding Information:

This study was supported by the grants of Small Project Funding (HKU-200807176136), Simon K.Y. Lee Endowed Professorship Research Fund, and the Outstanding Researcher Award Fund of the University of Hong Kong, and the Science and Technology Programme of Guangzhou, China (2008J1-C261-3).

References

 

DC FieldValueLanguage
dc.contributor.authorZou, Ben_HK
dc.contributor.authorChim, CSen_HK
dc.contributor.authorPang, Ren_HK
dc.contributor.authorZeng, Hen_HK
dc.contributor.authorDai, Yen_HK
dc.contributor.authorZhang, Ren_HK
dc.contributor.authorLam, CSCen_HK
dc.contributor.authorTan, VPYen_HK
dc.contributor.authorHung, IFNen_HK
dc.contributor.authorLan, HYen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2011-08-26T14:23:59Z-
dc.date.available2011-08-26T14:23:59Z-
dc.date.issued2012en_HK
dc.identifier.citationMolecular Carcinogenesis, 2012, v. 51 n. 5, p. 422-432en_HK
dc.identifier.issn0899-1987en_HK
dc.identifier.urihttp://hdl.handle.net/10722/137367-
dc.description.abstractThe role of X chromosome-linked inhibitor of apoptosis protein (XIAP)-associated factor 1 (XAF1) in mediating apoptosis has been reported but the underlying mechanism remains unclear. The present study was designed to examine the putative interaction between XAF1 and p53 and the functional importance of this interaction in regulation of apoptosis in human gastric and colon cancer cells. We first identified XAF1 as a novel target gene of p53 by the chromatin immunoprecipitation (CHIP) assay and demonstrated that wild-type p53, but not mutant p53, down-regulated XAF1 at both mRNA and protein levels, which acted mostly under the condition of high expression of XAF1 and was associated with the physical interaction between p53 and the XAF1 promoter. We also found that the over-expression of XAF1 led to activation of wild-type p53 via post-translational modification in cells with or without DNA damage, which resulting in p53 nuclear accumulation and its increased transcriptional activity and enhancing p53-dependent apoptosis. These findings suggest that a potential novel feedback loop exists between XAF1 and wild-type p53. © 2011 Wiley Periodicals, Inc.en_HK
dc.languageengen_US
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0899-1987/en_HK
dc.relation.ispartofMolecular Carcinogenesisen_HK
dc.subjectApoptosisen_HK
dc.subjectColon canceren_HK
dc.subjectGastric canceren_HK
dc.subjectP53en_HK
dc.subjectXAF1en_HK
dc.subject.meshApoptosis - geneticsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshColonic Neoplasms - genetics - metabolismen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntracellular Signaling Peptides and Proteins - genetics - metabolismen_HK
dc.subject.meshNeoplasm Proteins - genetics - metabolismen_HK
dc.subject.meshPromoter Regions, Geneticen_HK
dc.subject.meshProtein Processing, Post-Translational - geneticsen_HK
dc.subject.meshStomach Neoplasms - genetics - metabolismen_HK
dc.subject.meshTumor Suppressor Protein p53 - genetics - metabolismen_HK
dc.titleXIAP-associated factor 1 (XAF1), a novel target of p53, enhances p53-mediated apoptosis via post-translational modificationen_HK
dc.typeArticleen_HK
dc.identifier.emailChim, CS: jcschim@hku.hken_HK
dc.identifier.emailPang, R: robertap@hkucc.hku.hken_HK
dc.identifier.emailTan, VPY: vpytan@hku.hken_HK
dc.identifier.emailHung, IFN: ivanhung@hkucc.hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityChim, CS=rp00408en_HK
dc.identifier.authorityPang, R=rp00274en_HK
dc.identifier.authorityTan, VPY=rp01458en_HK
dc.identifier.authorityHung, IFN=rp00508en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/mc.20807en_HK
dc.identifier.pmid21678496en_HK
dc.identifier.scopuseid_2-s2.0-84859776957en_HK
dc.identifier.hkuros189629en_US
dc.identifier.hkuros173757-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84859776957&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume51en_HK
dc.identifier.issue5en_HK
dc.identifier.spage422en_HK
dc.identifier.epage432en_HK
dc.identifier.isiWOS:000302623000006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZou, B=35228257300en_HK
dc.identifier.scopusauthoridChim, CS=7004597253en_HK
dc.identifier.scopusauthoridPang, R=7004376659en_HK
dc.identifier.scopusauthoridZeng, H=35764158700en_HK
dc.identifier.scopusauthoridDai, Y=7401512993en_HK
dc.identifier.scopusauthoridZhang, R=9842860900en_HK
dc.identifier.scopusauthoridLam, CSC=35332626500en_HK
dc.identifier.scopusauthoridTan, VPY=24449627600en_HK
dc.identifier.scopusauthoridHung, IFN=7006103457en_HK
dc.identifier.scopusauthoridLan, HY=35783008500en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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