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Article: Non-steroidal anti-inflammatory drugs induce apoptosis in gastric cancer cells through up-regulation of bax and bak
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TitleNon-steroidal anti-inflammatory drugs induce apoptosis in gastric cancer cells through up-regulation of bax and bak
 
AuthorsZhou, XM2 1
Wong, BCY2
Fan, XM2
Zhang, HB1
Lin, MCM2
Kung, HF2
Fan, DM1
Lam, SK2
 
Issue Date2001
 
PublisherOxford University Press. The Journal's web site is located at http://carcin.oxfordjournals.org/
 
CitationCarcinogenesis, 2001, v. 22 n. 9, p. 1393-1397 [How to Cite?]
DOI: http://dx.doi.org/11532860
 
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.
 
ISSN0143-3334
2013 Impact Factor: 5.266
 
DOIhttp://dx.doi.org/11532860
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorZhou, XM
 
dc.contributor.authorWong, BCY
 
dc.contributor.authorFan, XM
 
dc.contributor.authorZhang, HB
 
dc.contributor.authorLin, MCM
 
dc.contributor.authorKung, HF
 
dc.contributor.authorFan, DM
 
dc.contributor.authorLam, SK
 
dc.date.accessioned2012-10-08T03:09:54Z
 
dc.date.available2012-10-08T03:09:54Z
 
dc.date.issued2001
 
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.
 
dc.description.natureLink_to_OA_fulltext
 
dc.identifier.citationCarcinogenesis, 2001, v. 22 n. 9, p. 1393-1397 [How to Cite?]
DOI: http://dx.doi.org/11532860
 
dc.identifier.doihttp://dx.doi.org/11532860
 
dc.identifier.epage1397
 
dc.identifier.hkuros68762
 
dc.identifier.issn0143-3334
2013 Impact Factor: 5.266
 
dc.identifier.issue9
 
dc.identifier.pmid11532860
 
dc.identifier.scopuseid_2-s2.0-0034806996
 
dc.identifier.spage1393
 
dc.identifier.urihttp://hdl.handle.net/10722/167678
 
dc.identifier.volume22
 
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.subject.meshAnti-Inflammatory Agents, Non-Steroidal - Pharmacology
 
dc.subject.meshApoptosis - Drug Effects - Physiology
 
dc.subject.meshAspirin - Pharmacology
 
dc.subject.meshCaspase 3
 
dc.subject.meshCaspases - Antagonists & Inhibitors - Biosynthesis - Genetics
 
dc.subject.meshCell Division - Drug Effects - Physiology
 
dc.subject.meshGene Expression Regulation, Neoplastic
 
dc.subject.meshHumans
 
dc.subject.meshIndomethacin - Pharmacology
 
dc.subject.meshMembrane Proteins - Biosynthesis - Genetics
 
dc.subject.meshPoly(Adp-Ribose) Polymerases - Biosynthesis - Genetics
 
dc.subject.meshProto-Oncogene Proteins - Biosynthesis - Genetics
 
dc.subject.meshProto-Oncogene Proteins C-Bcl-2 - Biosynthesis - Genetics
 
dc.subject.meshStomach Neoplasms - Genetics - Metabolism - Pathology
 
dc.subject.meshTumor Cells, Cultured
 
dc.subject.meshUp-Regulation - Drug Effects
 
dc.subject.meshBcl-2 Homologous Antagonist-Killer Protein
 
dc.subject.meshBcl-2-Associated X Protein
 
dc.subject.meshBcl-X Protein
 
dc.titleNon-steroidal anti-inflammatory drugs induce apoptosis in gastric cancer cells through up-regulation of bax and bak
 
dc.typeArticle
 
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Author Affiliations
  1. Xijing Hospital
  2. The University of Hong Kong