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Article: Melatonin-induced inhibition of proliferation and G 1/S cell cycle transition delay of human choriocarcinoma JAr cells: Possible involvement of MT 2 (MEL(1B)) receptor

TitleMelatonin-induced inhibition of proliferation and G 1/S cell cycle transition delay of human choriocarcinoma JAr cells: Possible involvement of MT 2 (MEL(1B)) receptor
Authors
Issue Date1999
PublisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPI
Citation
Journal Of Pineal Research, 1999, v. 27 n. 3, p. 183-192 How to Cite?
AbstractMelatonin, the pineal neurohormone, is an evolutionarily conserved photoperiodic signaling molecule with diverse functions that include the entrainment of human circadian rhythms. Although evidence supporting a direct inhibitory action of melatonin on human cancer cell proliferation exists in the literature, the molecular and cellular signaling mechanisms involved are largely undefined. In our study, significant inhibition of human choriocarcinoma JAr cell proliferation at physiological and pharmacological concentrations of melatonin was observed. 2-Iodomelatonin, a high affinity melatonin receptor agonist, was more potent than melatonin in inhibiting JAr cell proliferation. In addition, the presence of putative melatonin receptors in choriocarcinoma was suggested by the demonstration of specific 2-[ 125I]iodomelatonin binding to the tumor. Interestingly, the selective MT 2 melatonin receptor ligand, 4-phenyl-2-propionamidotetraline (4-P-PDOT), was found to exert not only concentration-dependent anti-proliferative actions on JAr cells, but also additive effects with melatonin in inhibiting JAr cell proliferation. Furthermore, MT 2 melatonin receptor gene expression by JAr cells was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization (ISH). Taken together, our data suggest that the reported anti-proliferative action of melatonin on human choriocarcinoma JAr cells may be mediated, in part, by MT 2 melatonin receptor. Moreover, analysis of melatonin effect on cell cycle kinetics indicated that G 1/S transition delay may underlie the observed inhibition of choriocarcinoma cell proliferation by melatonin.
Persistent Identifierhttp://hdl.handle.net/10722/171666
ISSN
2015 Impact Factor: 9.314
2015 SCImago Journal Rankings: 2.655
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShiu, SYWen_US
dc.contributor.authorLi, Len_US
dc.contributor.authorXu, JNen_US
dc.contributor.authorPang, CSen_US
dc.contributor.authorWong, JTYen_US
dc.contributor.authorPang, SFen_US
dc.date.accessioned2012-10-30T06:16:15Z-
dc.date.available2012-10-30T06:16:15Z-
dc.date.issued1999en_US
dc.identifier.citationJournal Of Pineal Research, 1999, v. 27 n. 3, p. 183-192en_US
dc.identifier.issn0742-3098en_US
dc.identifier.urihttp://hdl.handle.net/10722/171666-
dc.description.abstractMelatonin, the pineal neurohormone, is an evolutionarily conserved photoperiodic signaling molecule with diverse functions that include the entrainment of human circadian rhythms. Although evidence supporting a direct inhibitory action of melatonin on human cancer cell proliferation exists in the literature, the molecular and cellular signaling mechanisms involved are largely undefined. In our study, significant inhibition of human choriocarcinoma JAr cell proliferation at physiological and pharmacological concentrations of melatonin was observed. 2-Iodomelatonin, a high affinity melatonin receptor agonist, was more potent than melatonin in inhibiting JAr cell proliferation. In addition, the presence of putative melatonin receptors in choriocarcinoma was suggested by the demonstration of specific 2-[ 125I]iodomelatonin binding to the tumor. Interestingly, the selective MT 2 melatonin receptor ligand, 4-phenyl-2-propionamidotetraline (4-P-PDOT), was found to exert not only concentration-dependent anti-proliferative actions on JAr cells, but also additive effects with melatonin in inhibiting JAr cell proliferation. Furthermore, MT 2 melatonin receptor gene expression by JAr cells was demonstrated by reverse transcription-polymerase chain reaction (RT-PCR) and in situ hybridization (ISH). Taken together, our data suggest that the reported anti-proliferative action of melatonin on human choriocarcinoma JAr cells may be mediated, in part, by MT 2 melatonin receptor. Moreover, analysis of melatonin effect on cell cycle kinetics indicated that G 1/S transition delay may underlie the observed inhibition of choriocarcinoma cell proliferation by melatonin.en_US
dc.languageengen_US
dc.publisherBlackwell Munksgaard. The Journal's web site is located at http://www.blackwellpublishing.com/journals/JPIen_US
dc.relation.ispartofJournal of Pineal Researchen_US
dc.subject.meshCell Division - Drug Effectsen_US
dc.subject.meshChoriocarcinoma - Metabolism - Pathologyen_US
dc.subject.meshEpididymis - Cytologyen_US
dc.subject.meshEpithelial Cells - Cytologyen_US
dc.subject.meshG1 Phaseen_US
dc.subject.meshHumansen_US
dc.subject.meshIn Situ Hybridizationen_US
dc.subject.meshMaleen_US
dc.subject.meshMelatonin - Analogs & Derivatives - Metabolism - Pharmacologyen_US
dc.subject.meshReceptors, Cell Surface - Physiologyen_US
dc.subject.meshReceptors, Cytoplasmic And Nuclear - Physiologyen_US
dc.subject.meshReceptors, Melatoninen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshS Phaseen_US
dc.subject.meshTetrahydronaphthalenes - Pharmacologyen_US
dc.subject.meshTumor Cells, Cultureden_US
dc.titleMelatonin-induced inhibition of proliferation and G 1/S cell cycle transition delay of human choriocarcinoma JAr cells: Possible involvement of MT 2 (MEL(1B)) receptoren_US
dc.typeArticleen_US
dc.identifier.emailShiu, SYW:sywshiu@hkucc.hku.hken_US
dc.identifier.emailPang, SF: hrmypsf@hkucc.hku.hk-
dc.identifier.authorityShiu, SYW=rp00384en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1111/j.1600-079X.1999.tb00614.xen_US
dc.identifier.pmid10535768-
dc.identifier.scopuseid_2-s2.0-0032848858en_US
dc.identifier.hkuros51389-
dc.identifier.hkuros46320-
dc.identifier.hkuros58161-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032848858&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume27en_US
dc.identifier.issue3en_US
dc.identifier.spage183en_US
dc.identifier.epage192en_US
dc.identifier.isiWOS:000083250200008-
dc.publisher.placeDenmarken_US
dc.identifier.scopusauthoridShiu, SYW=7005550655en_US
dc.identifier.scopusauthoridLi, L=36985974800en_US
dc.identifier.scopusauthoridXu, JN=7407009328en_US
dc.identifier.scopusauthoridPang, CS=7201425191en_US
dc.identifier.scopusauthoridWong, JTY=24467064200en_US
dc.identifier.scopusauthoridPang, SF=7402528719en_US

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