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Article: Non-steroidal anti-inflammatory drug-induced apoptosis in gastric cancer cells is blocked by protein kinase C activation through inhibition of c-myc

TitleNon-steroidal anti-inflammatory drug-induced apoptosis in gastric cancer cells is blocked by protein kinase C activation through inhibition of c-myc
Authors
Issue Date1999
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjc
Citation
British Journal Of Cancer, 1999, v. 79 n. 3-4, p. 393-400 How to Cite?
AbstractApoptosis plays a major role in gastrointestinal epithelial cell turnover, ulcerogenesis and tumorigenesis. We have examined apoptosis induction by non-steroidal anti-inflammatory drugs (NSAIDs) in human gastric (AGS) cancer cells and the role of protein kinase C (PKC) and apoptosis-related oncogenes. After treatment with aspirin or indomethacin, cell growth was quantified by MTT assay, and apoptosis was determined by acridine orange staining, DNA fragmentation and flow cytometry. The mRNA and protein of p53, p21(waf1/cip1) and c-myc was detected by Northern and Western blotting respectively. The influence of PKC on indomethacin-induced apoptosis was determined by co-incubation of 12-O-tetradecanoylphorbol 13-acetate (TPA). The role of c-myc was determined using its antisense oligonucleotides. The results showed that both aspirin and indomethacin inhibited cell growth and induced apoptosis of AGS cells in a dose- and time-dependent manner, without altering the cell cycle. Indomethacin increased c-myc mRNA and protein, whereas p53 and p21(waf1/cip1) were unchanged. Down-regulation of c-myc by its antisense oligonucleotides reduced apoptosis induction by indomethacin. TPA could inhibit indomethacin-induced apoptosis and accumulate cells in G 2/M. Overexpression of c-myc was inhibited by TPA and p21(waf1/cip1) mRNA increased. In conclusion, NSAIDs induce apoptosis in gastric cancer cells which may be mediated by up-regulation of c-myc proto-oncogene. PKC activation can abrogate the effects of NSAIDs by decreasing c-myc expression.
Persistent Identifierhttp://hdl.handle.net/10722/78517
ISSN
2015 Impact Factor: 5.569
2015 SCImago Journal Rankings: 2.939
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhu, GHen_HK
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorEggo, MCen_HK
dc.contributor.authorChing, CKen_HK
dc.contributor.authorYuen, STen_HK
dc.contributor.authorChan, EYTen_HK
dc.contributor.authorLai, KCen_HK
dc.contributor.authorLam, SKen_HK
dc.date.accessioned2010-09-06T07:43:46Z-
dc.date.available2010-09-06T07:43:46Z-
dc.date.issued1999en_HK
dc.identifier.citationBritish Journal Of Cancer, 1999, v. 79 n. 3-4, p. 393-400en_HK
dc.identifier.issn0007-0920en_HK
dc.identifier.urihttp://hdl.handle.net/10722/78517-
dc.description.abstractApoptosis plays a major role in gastrointestinal epithelial cell turnover, ulcerogenesis and tumorigenesis. We have examined apoptosis induction by non-steroidal anti-inflammatory drugs (NSAIDs) in human gastric (AGS) cancer cells and the role of protein kinase C (PKC) and apoptosis-related oncogenes. After treatment with aspirin or indomethacin, cell growth was quantified by MTT assay, and apoptosis was determined by acridine orange staining, DNA fragmentation and flow cytometry. The mRNA and protein of p53, p21(waf1/cip1) and c-myc was detected by Northern and Western blotting respectively. The influence of PKC on indomethacin-induced apoptosis was determined by co-incubation of 12-O-tetradecanoylphorbol 13-acetate (TPA). The role of c-myc was determined using its antisense oligonucleotides. The results showed that both aspirin and indomethacin inhibited cell growth and induced apoptosis of AGS cells in a dose- and time-dependent manner, without altering the cell cycle. Indomethacin increased c-myc mRNA and protein, whereas p53 and p21(waf1/cip1) were unchanged. Down-regulation of c-myc by its antisense oligonucleotides reduced apoptosis induction by indomethacin. TPA could inhibit indomethacin-induced apoptosis and accumulate cells in G 2/M. Overexpression of c-myc was inhibited by TPA and p21(waf1/cip1) mRNA increased. In conclusion, NSAIDs induce apoptosis in gastric cancer cells which may be mediated by up-regulation of c-myc proto-oncogene. PKC activation can abrogate the effects of NSAIDs by decreasing c-myc expression.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/bjcen_HK
dc.relation.ispartofBritish Journal of Canceren_HK
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - pharmacologyen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshAspirin - pharmacologyen_HK
dc.subject.meshBlotting, Northernen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCell Cycle - drug effectsen_HK
dc.subject.meshDNA, Neoplasm - analysisen_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshGene Expression Regulation, Neoplastic - drug effectsen_HK
dc.subject.meshGenes, myc - geneticsen_HK
dc.subject.meshGenes, p53 - geneticsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIndomethacin - pharmacologyen_HK
dc.subject.meshProtein Kinase C - genetics - metabolismen_HK
dc.subject.meshRNA, Messenger - biosynthesisen_HK
dc.subject.meshStomach Neoplasms - genetics - physiopathologyen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleNon-steroidal anti-inflammatory drug-induced apoptosis in gastric cancer cells is blocked by protein kinase C activation through inhibition of c-mycen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0007-0920&volume=79&spage=393&epage=400&date=1999&atitle=Non-steroidal+anti-inflammatory+drug-induced+apoptosis+in+gastric+cancer+cells+is+blocked+by+protein+kinase+C+activation+through+inhibition+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.doi10.1038/sj.bjc.6690062en_HK
dc.identifier.pmid10027304-
dc.identifier.scopuseid_2-s2.0-0032928422en_HK
dc.identifier.hkuros39239en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032928422&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume79en_HK
dc.identifier.issue3-4en_HK
dc.identifier.spage393en_HK
dc.identifier.epage400en_HK
dc.identifier.isiWOS:000078165200003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridZhu, GH=7402633170en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridEggo, MC=7006000548en_HK
dc.identifier.scopusauthoridChing, CK=7102130825en_HK
dc.identifier.scopusauthoridYuen, ST=7103160927en_HK
dc.identifier.scopusauthoridChan, EYT=7401994013en_HK
dc.identifier.scopusauthoridLai, KC=7402135595en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK

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