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Article: Loss of XIAP sensitizes colon cancer cells to PPARγ independent antitumor effects of troglitazone and 15-PGJ2

TitleLoss of XIAP sensitizes colon cancer cells to PPARγ independent antitumor effects of troglitazone and 15-PGJ2
Authors
Qiao, LDai, YGu, QChan, KWMa, JLan, HYZou, BRocken, CEbert, MPAWong, BCY
KeywordsColon cancer
Ligands
PPARγ
Therapy
XIAP
Issue Date2008
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2008, v. 268 n. 2, p. 260-271 How to Cite?
DOI: http://dx.doi.org/10.1016/j.canlet.2008.04.003
AbstractWe investigated whether the anticancer effect of a combination of XIAP down-regulation and PPAR γ activation on colon cancer is PPARγ receptor dependent. HCT116-XIAP +/+ cells and HCT116-XIAP -/- cells were treated with troglitazone or 15-deoxy-Δ 12,14-prostaglandin J2 (15-PGJ2) with or without prior exposure to PPARγ inhibitor GW9662. Cell proliferation and apoptosis was evaluated. Athymic mice carrying HCT116-XIAP -/- cells-derived tumors were treated with troglitazone in the presence or absence of GW9662. Inhibition of cell proliferation and induction of apoptosis by troglitazone and 15-PGJ2 were more prominent in HCT116-XIAP -/- cells. PPARγ ligand-induced growth inhibition, apoptosis, caspase and PARP cleavage could not be blocked by GW9662. Troglitazone significantly retarded growth of xenograft tumors and this effect was not blocked by GW9662. Marked apoptosis and an up-regulation of E-cadherin were observed in xenograft tumor tissues, and GW9662 did not affect these effects. Thus, a combination of XIAP down-regulation and PPARγ ligands exert a significant anticancer effect in colon cancer via a PPARγ independent pathway. © 2008 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/148572
ISSN
0304-3835
2023 Impact Factor: 9.1
2023 SCImago Journal Rankings: 2.595
ISI Accession Number ID
WOS:000259898500009
References
References in Scopus

 

DC FieldValueLanguage
dc.contributor.authorQiao, Len_HK
dc.contributor.authorDai, Yen_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorMa, Jen_HK
dc.contributor.authorLan, HYen_HK
dc.contributor.authorZou, Ben_HK
dc.contributor.authorRocken, Cen_HK
dc.contributor.authorEbert, MPAen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2012-05-29T06:13:48Z-
dc.date.available2012-05-29T06:13:48Z-
dc.date.issued2008en_HK
dc.identifier.citationCancer Letters, 2008, v. 268 n. 2, p. 260-271en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148572-
dc.description.abstractWe investigated whether the anticancer effect of a combination of XIAP down-regulation and PPAR γ activation on colon cancer is PPARγ receptor dependent. HCT116-XIAP +/+ cells and HCT116-XIAP -/- cells were treated with troglitazone or 15-deoxy-Δ 12,14-prostaglandin J2 (15-PGJ2) with or without prior exposure to PPARγ inhibitor GW9662. Cell proliferation and apoptosis was evaluated. Athymic mice carrying HCT116-XIAP -/- cells-derived tumors were treated with troglitazone in the presence or absence of GW9662. Inhibition of cell proliferation and induction of apoptosis by troglitazone and 15-PGJ2 were more prominent in HCT116-XIAP -/- cells. PPARγ ligand-induced growth inhibition, apoptosis, caspase and PARP cleavage could not be blocked by GW9662. Troglitazone significantly retarded growth of xenograft tumors and this effect was not blocked by GW9662. Marked apoptosis and an up-regulation of E-cadherin were observed in xenograft tumor tissues, and GW9662 did not affect these effects. Thus, a combination of XIAP down-regulation and PPARγ ligands exert a significant anticancer effect in colon cancer via a PPARγ independent pathway. © 2008 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_US
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.-
dc.subjectColon canceren_HK
dc.subjectLigandsen_HK
dc.subjectPPARγen_HK
dc.subjectTherapyen_HK
dc.subjectXIAPen_HK
dc.subject.meshAnilides - Pharmacologyen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntineoplastic Agents - Pharmacologyen_US
dc.subject.meshApoptosis - Drug Effectsen_US
dc.subject.meshBlotting, Westernen_US
dc.subject.meshCaspases - Metabolismen_US
dc.subject.meshChromans - Pharmacologyen_US
dc.subject.meshColonic Neoplasms - Drug Therapy - Pathologyen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshHct116 Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshImmunohistochemistryen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Inbred Balb Cen_US
dc.subject.meshPpar Gamma - Analysis - Physiologyen_US
dc.subject.meshProstaglandin D2 - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshThiazolidinediones - Pharmacologyen_US
dc.subject.meshX-Linked Inhibitor Of Apoptosis Protein - Analysis - Antagonists & Inhibitors - Physiologyen_US
dc.titleLoss of XIAP sensitizes colon cancer cells to PPARγ independent antitumor effects of troglitazone and 15-PGJ2en_HK
dc.typeArticleen_HK
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.emailChan, KW: hrmtckw@hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.canlet.2008.04.003en_HK
dc.identifier.pmid18477501-
dc.identifier.scopuseid_2-s2.0-48549105519en_HK
dc.identifier.hkuros143396-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-48549105519&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume268en_HK
dc.identifier.issue2en_HK
dc.identifier.spage260en_HK
dc.identifier.epage271en_HK
dc.identifier.isiWOS:000259898500009-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridQiao, L=7202151719en_HK
dc.identifier.scopusauthoridDai, Y=7401512993en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridMa, J=35275386200en_HK
dc.identifier.scopusauthoridLan, HY=7102710832en_HK
dc.identifier.scopusauthoridZou, B=35228257300en_HK
dc.identifier.scopusauthoridRocken, C=7006367084en_HK
dc.identifier.scopusauthoridEbert, MPA=35239660600en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.issnl0304-3835-

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