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Article: Cyclooxygenase-2 Inhibitor (SC-236) Suppresses Activator Protein-1 through c-Jun NH2-Terminal Kinase

TitleCyclooxygenase-2 Inhibitor (SC-236) Suppresses Activator Protein-1 through c-Jun NH2-Terminal Kinase
Authors
Issue Date2004
PublisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastro
Citation
Gastroenterology, 2004, v. 126 n. 1 SUPPL. 1, p. 136-147 How to Cite?
AbstractBackground & Aims: Aspirin exerts antitumor effect partly through blocking tumor promoter-induced activator protein-1 (AP-1) activation. The aim of this study is to determine how specific COX-2 inhibitor SC-236 mediates antitumor effect by modulation of AP-1-signaling pathway. Methods: AP-1 transcriptional activity and DNA-binding activity were detected by luciferase reporter assay and gel shift assay, separately. Mitogen-activated protein kinase (MAPK) activation was determined by Western blot and in vitro kinase assay. Antisense oligonucleotide against c-Jun-N-terminal kinase (JNK) was used to suppress JNK expression. Results: We showed that SC-236 inhibited 12-O-tetradecanoylphorbol-13-acetate (PMA)-induced cell transformation in a dose-dependent manner in JB6 cells. At a dose range (12.5-50 μmol/L) that inhibited cell transformation, SC-236 also inhibited anchorage-independent cell growth and AP-1-activation in 3 gastric cancer cells, independent of COX-prostaglandin synthesis. SC-236 down-regulated c-Jun-NH2-terminal kinase phosphorylation and activity. Suppression of JNK activity reversed the inhibitory effect on AP-1 activity by SC-236 and suppressed gastric cancer cell growth, indicating that the inhibitory effect of SC-236 on AP-1 activation and cell growth was through interaction with JNK. Conclusions: The inhibitory effect on JNK-c-Jun/AP-1 activation contributes to the antitumor effect of COX-2-specific inhibitor, and inhibition of JNK activation may have a therapeutic benefit against gastric cancer.
Persistent Identifierhttp://hdl.handle.net/10722/77852
ISSN
2015 Impact Factor: 18.187
2015 SCImago Journal Rankings: 7.170
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, BCYen_HK
dc.contributor.authorJiang, XHen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorTu, SPen_HK
dc.contributor.authorCui, JTen_HK
dc.contributor.authorJiang, SHen_HK
dc.contributor.authorWong, WMen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorKung, HFen_HK
dc.date.accessioned2010-09-06T07:36:27Z-
dc.date.available2010-09-06T07:36:27Z-
dc.date.issued2004en_HK
dc.identifier.citationGastroenterology, 2004, v. 126 n. 1 SUPPL. 1, p. 136-147en_HK
dc.identifier.issn0016-5085en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77852-
dc.description.abstractBackground & Aims: Aspirin exerts antitumor effect partly through blocking tumor promoter-induced activator protein-1 (AP-1) activation. The aim of this study is to determine how specific COX-2 inhibitor SC-236 mediates antitumor effect by modulation of AP-1-signaling pathway. Methods: AP-1 transcriptional activity and DNA-binding activity were detected by luciferase reporter assay and gel shift assay, separately. Mitogen-activated protein kinase (MAPK) activation was determined by Western blot and in vitro kinase assay. Antisense oligonucleotide against c-Jun-N-terminal kinase (JNK) was used to suppress JNK expression. Results: We showed that SC-236 inhibited 12-O-tetradecanoylphorbol-13-acetate (PMA)-induced cell transformation in a dose-dependent manner in JB6 cells. At a dose range (12.5-50 μmol/L) that inhibited cell transformation, SC-236 also inhibited anchorage-independent cell growth and AP-1-activation in 3 gastric cancer cells, independent of COX-prostaglandin synthesis. SC-236 down-regulated c-Jun-NH2-terminal kinase phosphorylation and activity. Suppression of JNK activity reversed the inhibitory effect on AP-1 activity by SC-236 and suppressed gastric cancer cell growth, indicating that the inhibitory effect of SC-236 on AP-1 activation and cell growth was through interaction with JNK. Conclusions: The inhibitory effect on JNK-c-Jun/AP-1 activation contributes to the antitumor effect of COX-2-specific inhibitor, and inhibition of JNK activation may have a therapeutic benefit against gastric cancer.en_HK
dc.languageengen_HK
dc.publisherWB Saunders Co. The Journal's web site is located at http://www.elsevier.com/locate/gastroen_HK
dc.relation.ispartofGastroenterologyen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCyclooxygenase 2en_HK
dc.subject.meshCyclooxygenase 2 Inhibitorsen_HK
dc.subject.meshCyclooxygenase Inhibitors - administration & dosage - pharmacologyen_HK
dc.subject.meshDinoprostone - antagonists & inhibitorsen_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshEnzyme Activation - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIsoenzymes - antagonists & inhibitorsen_HK
dc.subject.meshJNK Mitogen-Activated Protein Kinasesen_HK
dc.subject.meshMembrane Proteinsen_HK
dc.subject.meshMitogen-Activated Protein Kinases - antagonists & inhibitorsen_HK
dc.subject.meshPhosphorylation - drug effectsen_HK
dc.subject.meshProstaglandin-Endoperoxide Synthasesen_HK
dc.subject.meshPyrazoles - administration & dosage - pharmacologyen_HK
dc.subject.meshStomach Neoplasms - pathologyen_HK
dc.subject.meshSulfonamides - administration & dosage - pharmacologyen_HK
dc.subject.meshTetradecanoylphorbol Acetate - pharmacologyen_HK
dc.subject.meshTranscription Factor AP-1 - antagonists & inhibitorsen_HK
dc.titleCyclooxygenase-2 Inhibitor (SC-236) Suppresses Activator Protein-1 through c-Jun NH2-Terminal Kinaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0016-5085&volume=126&spage=136&epage=147&date=2004&atitle=Cyclooxygenase-2+Inhibitor+(SC-236)+Suppresses+Activator+Protein-1+through+c-Jun+NH2-Terminal+Kinaseen_HK
dc.identifier.emailWong, BCY:bcywong@hku.hken_HK
dc.identifier.emailLin, MCM:mcllin@hkucc.hku.hken_HK
dc.identifier.emailYuen, MF:mfyuen@hkucc.hku.hken_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1053/j.gastro.2003.10.063en_HK
dc.identifier.pmid14699495-
dc.identifier.scopuseid_2-s2.0-9144219665en_HK
dc.identifier.hkuros85516en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-9144219665&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume126en_HK
dc.identifier.issue1 SUPPL. 1en_HK
dc.identifier.spage136en_HK
dc.identifier.epage147en_HK
dc.identifier.isiWOS:000187803300020-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.scopusauthoridJiang, XH=36089034900en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridTu, SP=7202726555en_HK
dc.identifier.scopusauthoridCui, JT=7401811557en_HK
dc.identifier.scopusauthoridJiang, SH=7404453122en_HK
dc.identifier.scopusauthoridWong, WM=7403972413en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridLam, SK=7402279473en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK

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