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Article: Non-steroidal anti-inflammatory drugs induce apoptosis in gastric cancer cells through up-regulation of bax and bak

TitleNon-steroidal anti-inflammatory drugs induce apoptosis in gastric cancer cells through up-regulation of bax and bak
Authors
Issue Date2001
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
Citation
Carcinogenesis, 2001, v. 22 n. 9, p. 1393-1397 How to Cite?
Abstract
Aspirin- and non-steroidal anti-inflammatory drug (NSAID)-induced apoptosis is one of the important mechanisms for their anti-tumour effect in gastric cancer. We aimed at determining the role of bcl-2 family proteins and caspases in the apoptotic process. Gastric cancer cell lines AGS (wild-type p53) and MKN-28 (mutant p53) were used. Cell proliferation was measured by MTT assay. Apoptosis was determined by acridine orange staining. Protein expressions were determined by western blotting. Aspirin and indomethacin inhibited cell proliferation and induced apoptosis in both cells. AGS cells were more sensitive compared with MKN-28 cells. The pro-apoptotic proteins bax and bak were overexpressed after treatment, while the protein level of bcl-2 remained unchanged. Apoptosis was accompanied by an increase in caspase-3 activity and cleavage of caspase-3 and poly(ADP-ribose) polymerase. Inhibition of caspase-3 rescued aspirin-induced apoptosis. Our results suggest that one of the major pathways which mediates the anti-tumour response of aspirin and indomethacin in gastric cancer cells is through up-regulation of bax and bak and activation of caspase-3. Bax and bak are important in the chemoprevention of gastric cancer.
Persistent Identifierhttp://hdl.handle.net/10722/167678
ISSN
2013 Impact Factor: 5.266
ISI Accession Number ID
References

 

Author Affiliations
  1. Xijing Hospital
  2. The University of Hong Kong
DC FieldValueLanguage
dc.contributor.authorZhou, XMen_US
dc.contributor.authorWong, BCYen_US
dc.contributor.authorFan, XMen_US
dc.contributor.authorZhang, HBen_US
dc.contributor.authorLin, MCMen_US
dc.contributor.authorKung, HFen_US
dc.contributor.authorFan, DMen_US
dc.contributor.authorLam, SKen_US
dc.date.accessioned2012-10-08T03:09:54Z-
dc.date.available2012-10-08T03:09:54Z-
dc.date.issued2001en_US
dc.identifier.citationCarcinogenesis, 2001, v. 22 n. 9, p. 1393-1397en_US
dc.identifier.issn0143-3334en_US
dc.identifier.urihttp://hdl.handle.net/10722/167678-
dc.description.abstractAspirin- and non-steroidal anti-inflammatory drug (NSAID)-induced apoptosis is one of the important mechanisms for their anti-tumour effect in gastric cancer. We aimed at determining the role of bcl-2 family proteins and caspases in the apoptotic process. Gastric cancer cell lines AGS (wild-type p53) and MKN-28 (mutant p53) were used. Cell proliferation was measured by MTT assay. Apoptosis was determined by acridine orange staining. Protein expressions were determined by western blotting. Aspirin and indomethacin inhibited cell proliferation and induced apoptosis in both cells. AGS cells were more sensitive compared with MKN-28 cells. The pro-apoptotic proteins bax and bak were overexpressed after treatment, while the protein level of bcl-2 remained unchanged. Apoptosis was accompanied by an increase in caspase-3 activity and cleavage of caspase-3 and poly(ADP-ribose) polymerase. Inhibition of caspase-3 rescued aspirin-induced apoptosis. Our results suggest that one of the major pathways which mediates the anti-tumour response of aspirin and indomethacin in gastric cancer cells is through up-regulation of bax and bak and activation of caspase-3. Bax and bak are important in the chemoprevention of gastric cancer.en_US
dc.languageengen_US
dc.publisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/en_US
dc.relation.ispartofCarcinogenesisen_US
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - Pharmacologyen_US
dc.subject.meshApoptosis - Drug Effects - Physiologyen_US
dc.subject.meshAspirin - Pharmacologyen_US
dc.subject.meshCaspase 3en_US
dc.subject.meshCaspases - Antagonists & Inhibitors - Biosynthesis - Geneticsen_US
dc.subject.meshCell Division - Drug Effects - Physiologyen_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshHumansen_US
dc.subject.meshIndomethacin - Pharmacologyen_US
dc.subject.meshMembrane Proteins - Biosynthesis - Geneticsen_US
dc.subject.meshPoly(Adp-Ribose) Polymerases - Biosynthesis - Geneticsen_US
dc.subject.meshProto-Oncogene Proteins - Biosynthesis - Geneticsen_US
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Biosynthesis - Geneticsen_US
dc.subject.meshStomach Neoplasms - Genetics - Metabolism - Pathologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshUp-Regulation - Drug Effectsen_US
dc.subject.meshBcl-2 Homologous Antagonist-Killer Proteinen_US
dc.subject.meshBcl-2-Associated X Proteinen_US
dc.subject.meshBcl-X Proteinen_US
dc.titleNon-steroidal anti-inflammatory drugs induce apoptosis in gastric cancer cells through up-regulation of bax and baken_US
dc.typeArticleen_US
dc.identifier.emailWong, BCY:bcywong@hku.hken_US
dc.identifier.emailLin, MCM:mcllin@hkucc.hku.hken_US
dc.identifier.authorityWong, BCY=rp00429en_US
dc.identifier.authorityLin, MCM=rp00746en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1093/carcin/22.9.1393-
dc.identifier.pmid11532860en_US
dc.identifier.scopuseid_2-s2.0-0034806996en_US
dc.identifier.hkuros68762-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034806996&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume22en_US
dc.identifier.issue9en_US
dc.identifier.spage1393en_US
dc.identifier.epage1397en_US
dc.identifier.isiWOS:000171021100009-
dc.publisher.placeUnited Kingdomen_US
dc.identifier.scopusauthoridZhou, XM=7410092583en_US
dc.identifier.scopusauthoridWong, BCY=7402023340en_US
dc.identifier.scopusauthoridFan, XM=35187111100en_US
dc.identifier.scopusauthoridZhang, HB=7409200796en_US
dc.identifier.scopusauthoridLin, MCM=7404816359en_US
dc.identifier.scopusauthoridKung, HF=7402514190en_US
dc.identifier.scopusauthoridFan, DM=7202965595en_US
dc.identifier.scopusauthoridLam, SK=7402279473en_US

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