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Article: Differential apoptosis by indomethacin in gastric epithelial cells through the constitutive expression of wild-type p53 and/or up-regulation of c-myc

TitleDifferential apoptosis by indomethacin in gastric epithelial cells through the constitutive expression of wild-type p53 and/or up-regulation of c-myc
Authors
Issue Date1999
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm
Citation
Biochemical Pharmacology, 1999, v. 58 n. 1, p. 193-200 How to Cite?
AbstractNonsteroidal anti-inflammatory drug (NSAID)-induced apoptosis is considered to be an important mechanism in the antineoplastic effects and damage produced by the drugs in the gastrointestinal tract. In this study, two different gastric cancer cell lines, MKN28 (mutant-type p53) and AGS (wild-type p53), were compared as to growth inhibition, apoptosis, and cell cycle and apoptosis-related gene expression in response to indomethacin treatment. Cell growth was measured by MTT (3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide) assay. Apoptosis was characterized by acridine orange staining and DNA fragmentation, and cell cycle kinetics by flow cytometry. The mRNA and protein levels of p53, p21(waf1/cip1), and c-myc were determined by Northern and Western blotting. The results showed that indomethacin initiated growth inhibition and apoptosis in both cell lines without cell cycle shifting. AGS cells were more sensitive to growth inhibitory activity and apoptosis of indomethacin than MKN28 cells. In MKN28 cells, the levels of p53, p21(waf1/cip1), and c-myc mRNA remained unchanged over the 24-hr treatment with indomethacin, but the p53 protein level was elevated after 4 hr. There was no change in the p21(waf1/cip1) and c-myc protein levels in the MKN28 cells. In AGS cells, a progressive increase in c-myc mRNA and protein levels was noted, while p53 and p21(waf1/cip1) remained unchanged. It can be concluded that wild-type p53 and/or up-regulation of c-myc is associated with indomethacin-mediated differential apoptosis in gastric epithelial cells. Copyright (C) 1999 Elsevier Science Inc.
Persistent Identifierhttp://hdl.handle.net/10722/76550
ISSN
2015 Impact Factor: 5.091
2015 SCImago Journal Rankings: 2.263
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhu, GHen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorChing, CKen_HK
dc.contributor.authorLai, KCen_HK
dc.contributor.authorLam, SKen_HK
dc.date.accessioned2010-09-06T07:22:26Z-
dc.date.available2010-09-06T07:22:26Z-
dc.date.issued1999en_HK
dc.identifier.citationBiochemical Pharmacology, 1999, v. 58 n. 1, p. 193-200en_HK
dc.identifier.issn0006-2952en_HK
dc.identifier.urihttp://hdl.handle.net/10722/76550-
dc.description.abstractNonsteroidal anti-inflammatory drug (NSAID)-induced apoptosis is considered to be an important mechanism in the antineoplastic effects and damage produced by the drugs in the gastrointestinal tract. In this study, two different gastric cancer cell lines, MKN28 (mutant-type p53) and AGS (wild-type p53), were compared as to growth inhibition, apoptosis, and cell cycle and apoptosis-related gene expression in response to indomethacin treatment. Cell growth was measured by MTT (3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide) assay. Apoptosis was characterized by acridine orange staining and DNA fragmentation, and cell cycle kinetics by flow cytometry. The mRNA and protein levels of p53, p21(waf1/cip1), and c-myc were determined by Northern and Western blotting. The results showed that indomethacin initiated growth inhibition and apoptosis in both cell lines without cell cycle shifting. AGS cells were more sensitive to growth inhibitory activity and apoptosis of indomethacin than MKN28 cells. In MKN28 cells, the levels of p53, p21(waf1/cip1), and c-myc mRNA remained unchanged over the 24-hr treatment with indomethacin, but the p53 protein level was elevated after 4 hr. There was no change in the p21(waf1/cip1) and c-myc protein levels in the MKN28 cells. In AGS cells, a progressive increase in c-myc mRNA and protein levels was noted, while p53 and p21(waf1/cip1) remained unchanged. It can be concluded that wild-type p53 and/or up-regulation of c-myc is associated with indomethacin-mediated differential apoptosis in gastric epithelial cells. Copyright (C) 1999 Elsevier Science Inc.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharmen_HK
dc.relation.ispartofBiochemical Pharmacologyen_HK
dc.rightsBiochemical Pharmacology. Copyright © Elsevier Inc.en_HK
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - pharmacologyen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshCell Cycle - drug effectsen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p21en_HK
dc.subject.meshCyclins - biosynthesis - physiologyen_HK
dc.subject.meshEpithelial Cells - drug effects - pathologyen_HK
dc.subject.meshGene Expression - drug effectsen_HK
dc.subject.meshGenes, myc - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIndomethacin - pharmacologyen_HK
dc.subject.meshRNA, Messenger - biosynthesis - drug effectsen_HK
dc.subject.meshStomach - pathologyen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshTumor Suppressor Protein p53 - biosynthesis - physiologyen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleDifferential apoptosis by indomethacin in gastric epithelial cells through the constitutive expression of wild-type p53 and/or up-regulation of c-mycen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0006-2952&volume=58&spage=193&epage=200&date=1998&atitle=Differential+apoptosis+by+indomethacin+in+gastric+epithelial+cells+through+the+constitutive+expression+of+wild-type+p53+and/or+up-regulation+of+c-mycen_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0006-2952(99)00058-1en_HK
dc.identifier.pmid10403534-
dc.identifier.scopuseid_2-s2.0-0033169028en_HK
dc.identifier.hkuros41166en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033169028&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume58en_HK
dc.identifier.issue1en_HK
dc.identifier.spage193en_HK
dc.identifier.epage200en_HK
dc.identifier.isiWOS:000080689600020-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhu, GH=7402633170en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridChing, CK=7102130825en_HK
dc.identifier.scopusauthoridLai, KC=7402135595en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK

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