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

TitleActivation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric cancer
Authors
Issue Date2005
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2005, v. 26 n. 3, p. 541-546 How to Cite?
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.
Persistent Identifierhttp://hdl.handle.net/10722/78004
ISSN
2021 Impact Factor: 4.741
2020 SCImago Journal Rankings: 1.688
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorGu, Qen_HK
dc.contributor.authorDe Wang, Jen_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorHe, Hen_HK
dc.contributor.authorZou, Ben_HK
dc.contributor.authorTu, SPen_HK
dc.contributor.authorYang, Yen_HK
dc.contributor.authorLiu, XGen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorChan, AOOen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-06T07:38:07Z-
dc.date.available2010-09-06T07:38:07Z-
dc.date.issued2005en_HK
dc.identifier.citationCarcinogenesis, 2005, v. 26 n. 3, p. 541-546en_HK
dc.identifier.issn0143-3334en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78004-
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.en_HK
dc.languageengen_HK
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_HK
dc.relation.ispartofCarcinogenesisen_HK
dc.rightsCarcinogenesis. Copyright © Oxford University Press.en_HK
dc.titleActivation of the caspase-8/Bid and Bax pathways in aspirin-induced apoptosis in gastric canceren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0143-3334&volume=26&issue=3&spage=541&epage=546&date=2005&atitle=Activation+of+the+Caspase-8/Bid+and+Bax+Pathways+in+Aspirin-Induced+Apoptosis+in+Gastric+Canceren_HK
dc.identifier.emailDe Wang, J: jidewang@gmail.comen_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.emailYuen, MF: mfyuen@hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityDe Wang, J=rp00491en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1093/carcin/bgh345en_HK
dc.identifier.scopuseid_2-s2.0-16244417810en_HK
dc.identifier.hkuros97452en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-16244417810&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume26en_HK
dc.identifier.issue3en_HK
dc.identifier.spage541en_HK
dc.identifier.epage546en_HK
dc.identifier.isiWOS:000227242400004-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridDe Wang, J=35309087500en_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridHe, H=36185495900en_HK
dc.identifier.scopusauthoridZou, B=35228257300en_HK
dc.identifier.scopusauthoridTu, SP=7202726555en_HK
dc.identifier.scopusauthoridYang, Y=8675011000en_HK
dc.identifier.scopusauthoridLiu, XG=26643623200en_HK
dc.identifier.scopusauthoridLam, SK=55424391900en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridChan, AOO=7403167965en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.citeulike104748-
dc.identifier.issnl0143-3334-

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