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Article: XIAP-associated factor 1 (XAF1), a novel target of p53, enhances p53-mediated apoptosis via post-translational modification
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TitleXIAP-associated factor 1 (XAF1), a novel target of p53, enhances p53-mediated apoptosis via post-translational modification
 
AuthorsZou, B2 1
Chim, CS1
Pang, R1
Zeng, H2
Dai, Y1
Zhang, R1
Lam, CSC1
Tan, VPY1
Hung, IFN1
Lan, HY3
Wong, BCY1
 
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/
 
CitationMolecular Carcinogenesis, 2012, v. 51 n. 5, p. 422-432 [How to Cite?]
DOI: http://dx.doi.org/10.1002/mc.20807
 
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.
 
ISSN0899-1987
2013 Impact Factor: 4.770
 
DOIhttp://dx.doi.org/10.1002/mc.20807
 
ISI Accession Number IDWOS:000302623000006
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).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorZou, B
 
dc.contributor.authorChim, CS
 
dc.contributor.authorPang, R
 
dc.contributor.authorZeng, H
 
dc.contributor.authorDai, Y
 
dc.contributor.authorZhang, R
 
dc.contributor.authorLam, CSC
 
dc.contributor.authorTan, VPY
 
dc.contributor.authorHung, IFN
 
dc.contributor.authorLan, HY
 
dc.contributor.authorWong, BCY
 
dc.date.accessioned2011-08-26T14:23:59Z
 
dc.date.available2011-08-26T14:23:59Z
 
dc.date.issued2012
 
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.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationMolecular Carcinogenesis, 2012, v. 51 n. 5, p. 422-432 [How to Cite?]
DOI: http://dx.doi.org/10.1002/mc.20807
 
dc.identifier.doihttp://dx.doi.org/10.1002/mc.20807
 
dc.identifier.epage432
 
dc.identifier.hkuros189629
 
dc.identifier.hkuros173757
 
dc.identifier.isiWOS:000302623000006
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).

 
dc.identifier.issn0899-1987
2013 Impact Factor: 4.770
 
dc.identifier.issue5
 
dc.identifier.pmid21678496
 
dc.identifier.scopuseid_2-s2.0-84859776957
 
dc.identifier.spage422
 
dc.identifier.urihttp://hdl.handle.net/10722/137367
 
dc.identifier.volume51
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0899-1987/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofMolecular Carcinogenesis
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshApoptosis - genetics
 
dc.subject.meshCell Line, Tumor
 
dc.subject.meshColonic Neoplasms - genetics - metabolism
 
dc.subject.meshGene Expression Regulation, Neoplastic
 
dc.subject.meshHumans
 
dc.subject.meshIntracellular Signaling Peptides and Proteins - genetics - metabolism
 
dc.subject.meshNeoplasm Proteins - genetics - metabolism
 
dc.subject.meshPromoter Regions, Genetic
 
dc.subject.meshProtein Processing, Post-Translational - genetics
 
dc.subject.meshStomach Neoplasms - genetics - metabolism
 
dc.subject.meshTumor Suppressor Protein p53 - genetics - metabolism
 
dc.subjectApoptosis
 
dc.subjectColon cancer
 
dc.subjectGastric cancer
 
dc.subjectP53
 
dc.subjectXAF1
 
dc.titleXIAP-associated factor 1 (XAF1), a novel target of p53, enhances p53-mediated apoptosis via post-translational modification
 
dc.typeArticle
 
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Author Affiliations
  1. The University of Hong Kong
  2. Guangzhou Medical College
  3. Chinese University of Hong Kong