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Article: κ-Opioid receptor potentiates apoptosis via a phospholipase C pathway in the CNE2 human epithelial tumor cell line

Titleκ-Opioid receptor potentiates apoptosis via a phospholipase C pathway in the CNE2 human epithelial tumor cell line
Authors
Issue Date2000
PublisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbamcr
Citation
Biochimica Et Biophysica Acta - Molecular Cell Research, 2000, v. 1499 n. 1-2, p. 49-62 How to Cite?
AbstractThe mechanism by which κ-opioid receptor (κor) modulated apoptosis was investigated in CNE2 human epithelial tumor cells. Induction of these cells to undergo apoptosis with staurosporine was associated with a massive increase in intracellular cAMP level. The inhibition of the increase in cAMP partially inhibited apoptosis as evidenced by a reduction of PARP and caspase-3 cleavage. Accordingly, a low but significant level of apoptosis is induced in these cells by the elevation of cAMP through the addition of forskolin and isobutylmethylxanthine. The existence of a cAMP-dependent and a cAMP-independent apoptotic pathway is therefore suggested. Receptor binding studies, RT-PCR experiments and Western blot analysis demonstrated the presence of type 1 κor in the CNE2 cells. Stimulation of κor in these cells resulted in the production of inositol (1,4,5)-trisphosphate, reduction of cAMP level and a marked enhancement of staurosporine-induced apoptosis. The potentiation of apoptosis by κor was prevented by inhibition of phospholipase C but was slightly enhanced by the presence of the active cAMP analogues, 8-CPT-cAMP and dibutyryl-cAMP. These data demonstrate for the first time that the phospholipase C pathway activated by type 1 κor expressed by cancer cells is involved in the potentiation of apoptosis. (C) 2000 Elsevier Science B.V.
Persistent Identifierhttp://hdl.handle.net/10722/147454
ISSN
2015 Impact Factor: 5.128
2015 SCImago Journal Rankings: 3.043
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorDiao, CTMen_US
dc.contributor.authorLi, Len_US
dc.contributor.authorLau, SYen_US
dc.contributor.authorWong, TMen_US
dc.contributor.authorWong, NSen_US
dc.date.accessioned2012-05-29T06:03:50Z-
dc.date.available2012-05-29T06:03:50Z-
dc.date.issued2000en_US
dc.identifier.citationBiochimica Et Biophysica Acta - Molecular Cell Research, 2000, v. 1499 n. 1-2, p. 49-62en_US
dc.identifier.issn0167-4889en_US
dc.identifier.urihttp://hdl.handle.net/10722/147454-
dc.description.abstractThe mechanism by which κ-opioid receptor (κor) modulated apoptosis was investigated in CNE2 human epithelial tumor cells. Induction of these cells to undergo apoptosis with staurosporine was associated with a massive increase in intracellular cAMP level. The inhibition of the increase in cAMP partially inhibited apoptosis as evidenced by a reduction of PARP and caspase-3 cleavage. Accordingly, a low but significant level of apoptosis is induced in these cells by the elevation of cAMP through the addition of forskolin and isobutylmethylxanthine. The existence of a cAMP-dependent and a cAMP-independent apoptotic pathway is therefore suggested. Receptor binding studies, RT-PCR experiments and Western blot analysis demonstrated the presence of type 1 κor in the CNE2 cells. Stimulation of κor in these cells resulted in the production of inositol (1,4,5)-trisphosphate, reduction of cAMP level and a marked enhancement of staurosporine-induced apoptosis. The potentiation of apoptosis by κor was prevented by inhibition of phospholipase C but was slightly enhanced by the presence of the active cAMP analogues, 8-CPT-cAMP and dibutyryl-cAMP. These data demonstrate for the first time that the phospholipase C pathway activated by type 1 κor expressed by cancer cells is involved in the potentiation of apoptosis. (C) 2000 Elsevier Science B.V.en_US
dc.languageengen_US
dc.publisherElsevier BV. The Journal's web site is located at http://www.elsevier.com/locate/bbamcren_US
dc.relation.ispartofBiochimica et Biophysica Acta - Molecular Cell Researchen_US
dc.subject.mesh3,4-Dichloro-N-Methyl-N-(2-(1-Pyrrolidinyl)-Cyclohexyl)-Benzeneacetamide, (Trans)-Isomer - Pharmacologyen_US
dc.subject.meshAdenine - Analogs & Derivatives - Pharmacologyen_US
dc.subject.meshApoptosisen_US
dc.subject.meshBase Sequenceen_US
dc.subject.meshBenzomorphans - Pharmacologyen_US
dc.subject.meshCell Membrane - Drug Effectsen_US
dc.subject.meshCyclic Amp - Metabolismen_US
dc.subject.meshDideoxyadenosine - Pharmacologyen_US
dc.subject.meshDrug Synergismen_US
dc.subject.meshEpithelial Cells - Physiologyen_US
dc.subject.meshEstrenes - Pharmacologyen_US
dc.subject.meshForskolin - Pharmacologyen_US
dc.subject.meshHumansen_US
dc.subject.meshMolecular Sequence Dataen_US
dc.subject.meshPyrrolidinones - Pharmacologyen_US
dc.subject.meshReceptors, Opioid, Kappa - Drug Effects - Physiologyen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshStaurosporine - Antagonists & Inhibitors - Pharmacologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.subject.meshType C Phospholipases - Antagonists & Inhibitors - Physiologyen_US
dc.titleκ-Opioid receptor potentiates apoptosis via a phospholipase C pathway in the CNE2 human epithelial tumor cell lineen_US
dc.typeArticleen_US
dc.identifier.emailWong, NS:nswong@hkucc.hku.hken_US
dc.identifier.authorityWong, NS=rp00340en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/S0167-4889(00)00107-5en_US
dc.identifier.pmid11118638-
dc.identifier.scopuseid_2-s2.0-0034639236en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034639236&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume1499en_US
dc.identifier.issue1-2en_US
dc.identifier.spage49en_US
dc.identifier.epage62en_US
dc.identifier.isiWOS:000166117700005-
dc.publisher.placeNetherlandsen_US
dc.identifier.scopusauthoridDiao, CTM=15738053400en_US
dc.identifier.scopusauthoridLi, L=15738409400en_US
dc.identifier.scopusauthoridLau, SY=7401596375en_US
dc.identifier.scopusauthoridWong, TM=7403531434en_US
dc.identifier.scopusauthoridWong, NS=7202836641en_US

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