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, XM1 2
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?]
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
2011 Impact Factor: 5.702
2011 SCImago Journal Rankings: 0.692
ReferencesReferences in Scopus
DC Field
Value
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_subscribed_fulltext
dc.identifier.citationCarcinogenesis, 2001, v. 22 n. 9, p. 1393-1397 [How to Cite?]
dc.identifier.epage1397
dc.identifier.issn0143-3334
2011 Impact Factor: 5.702
2011 SCImago Journal Rankings: 0.692
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
Author Affiliations
  1. Xijing Hospital
  2. The University of Hong Kong