Article: Activation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer

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TitleActivation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer
AuthorsGu, Q1 2
De Wang, J1
Xia, HHX1
Lin, MCM1
He, H1
Zou, B1
Tu, SP1
Yang, Y1
Liu, XG2
Lam, SK1
Wong, WM1
Chan, AOO1
Yuen, MF1
Kung, HF1
Wong, BCY1
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
CitationCarcinogenesis, 2005, v. 26 n. 3, p. 541-546 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgh345
AbstractAspirin-induced apoptosis is one of the important mechanisms for its antitumour effect against gastric cancer. We aimed at investigating the involvement of bcl-2 family members in the apoptotic pathway in gastric cancer. Gastric cancer cell line AGS and MKN-45 were observed as to cell growth inhibition and induction of apoptosis in response to treatment with aspirin. Cell proliferation was measured by MTT assay. Apoptosis was determined by 4′-6-diamidino-2-phenylindole staining. Protein expression was determined by western blotting. We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release. In addition, suppression of caspase-8 with the specific inhibitor z-IETD-fmk, as well as the pan-caspase inhibitor z-VAD-fmk, prevented Bid cleavage and subsequent apoptosis. The caspase inhibitors failed to abolish the effects on Bax activation. In conclusion, our results identify a role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer. © Oxford University Press 2004; all rights reserved.
ISSN0143-3334
2011 Impact Factor: 5.702
2011 SCImago Journal Rankings: 0.692
DOIhttp://dx.doi.org/10.1093/carcin/bgh345
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorGu, Q
dc.contributor.authorDe Wang, J
dc.contributor.authorXia, HHX
dc.contributor.authorLin, MCM
dc.contributor.authorHe, H
dc.contributor.authorZou, B
dc.contributor.authorTu, SP
dc.contributor.authorYang, Y
dc.contributor.authorLiu, XG
dc.contributor.authorLam, SK
dc.contributor.authorWong, WM
dc.contributor.authorChan, AOO
dc.contributor.authorYuen, MF
dc.contributor.authorKung, HF
dc.contributor.authorWong, BCY
dc.date.accessioned2010-09-06T07:38:07Z
dc.date.available2010-09-06T07:38:07Z
dc.date.issued2005
dc.description.abstractAspirin-induced apoptosis is one of the important mechanisms for its antitumour effect against gastric cancer. We aimed at investigating the involvement of bcl-2 family members in the apoptotic pathway in gastric cancer. Gastric cancer cell line AGS and MKN-45 were observed as to cell growth inhibition and induction of apoptosis in response to treatment with aspirin. Cell proliferation was measured by MTT assay. Apoptosis was determined by 4′-6-diamidino-2-phenylindole staining. Protein expression was determined by western blotting. We showed that aspirin activated caspase-8, caspase-9 and capase-3, cleaved and translocated Bid, induced a conformational change in and translocation of Bax and cytochrome c release. In addition, suppression of caspase-8 with the specific inhibitor z-IETD-fmk, as well as the pan-caspase inhibitor z-VAD-fmk, prevented Bid cleavage and subsequent apoptosis. The caspase inhibitors failed to abolish the effects on Bax activation. In conclusion, our results identify a role of caspase-8/Bid and activation of Bax as a novel mechanism for aspirin-induced apoptosis in gastric cancer. © Oxford University Press 2004; all rights reserved.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationCarcinogenesis, 2005, v. 26 n. 3, p. 541-546 [How to Cite?]
DOI: http://dx.doi.org/10.1093/carcin/bgh345
dc.identifier.citeulike104748
dc.identifier.doihttp://dx.doi.org/10.1093/carcin/bgh345
dc.identifier.epage546
dc.identifier.hkuros97452
dc.identifier.isiWOS:000227242400004
dc.identifier.issn0143-3334
2011 Impact Factor: 5.702
2011 SCImago Journal Rankings: 0.692
dc.identifier.issue3
dc.identifier.openurl
dc.identifier.scopuseid_2-s2.0-16244417810
dc.identifier.spage541
dc.identifier.urihttp://hdl.handle.net/10722/78004
dc.identifier.volume26
dc.languageeng
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
dc.publisher.placeUnited Kingdom
dc.relation.ispartofCarcinogenesis
dc.relation.referencesReferences in Scopus
dc.rightsCarcinogenesis. Copyright © Oxford University Press.
dc.titleActivation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong
  2. Peking University