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Article: Inhibition of malignant trophoblastic cell proliferation in vitro and in vivo by melatonin

TitleInhibition of malignant trophoblastic cell proliferation in vitro and in vivo by melatonin
Authors
KeywordsAnti-proliferation
Choriocarcinoma
Cyclin A
Melatonin
Nude mice
PCNA
Issue Date2000
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 2000, v. 67 n. 17, p. 2059-2074 How to Cite?
AbstractMelatonin inhibited thymidine incorporation into human choriocarcinoma JEG-3 cells at physiological and pharmacological concentrations in the present study. Gene expression of MT 2 receptor, but not that of mt 1 receptor, was detected in JEG-3 cells by reverse transcription-polymerase chain reaction (RT-PCR). The gene expression profile of the two human melatonin receptor subtypes in JEG-3 cells was identical to that previously reported for JAr cells, whose proliferation had also been shown to be similarly inhibited by physiological and pharmacological concentrations of melatonin. In contrast, melatonin had no effect on thymidine incorporation into 3A-Sub-E cells (a transformed trophoblast cell line), in which gene expression of both receptor subtypes could not be detected. The data suggest that in human placental trophoblasts, a correlation may exist between MT 2 receptor gene expression and the direct anti-proliferative action of melatonin. Although melatonin has been reported to induce G1/S delay in cell cycle progression of JAr cells, no significant changes in the percentages of JEG-3 cells in different cell cycle phases upon melatonin treatment was recorded by flow cytometric analysis. This indicates that G1/S transition delay is probably not an important cellular mechanism in the direct anti-proliferative action of melatonin on human JEG-3 cells in vitro. Furthermore, melatonin inhibited the growth of both JAr and JEG-3 xenograft tumors in athymic nude mice, and prolonged the survival of those animals that developed choriocarcinoma. While the number of apoptotic tumor cells was not increased by melatonin, the pineal hormone induced significant decreases in the numbers of JAr and JEG-3 cells expressing proliferating cell nuclear antigen (PCNA) and cyclin A in the tumors. Taking into account both the in vitro and in vivo findings, it is likely that the inhibitory effect of melatonin on choriocarcinoma JAr and JEG-3 cell proliferation in vivo is largely a direct action of the hormone on the tumor cells. (C) 2000 Elsevier Science Inc.
Persistent Identifierhttp://hdl.handle.net/10722/68281
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShiu, SYWen_HK
dc.contributor.authorXi, SCen_HK
dc.contributor.authorXu, JNen_HK
dc.contributor.authorMei, Len_HK
dc.contributor.authorPang, SFen_HK
dc.contributor.authorYao, KMen_HK
dc.contributor.authorWong, JTYen_HK
dc.date.accessioned2010-09-06T06:03:05Z-
dc.date.available2010-09-06T06:03:05Z-
dc.date.issued2000en_HK
dc.identifier.citationLife Sciences, 2000, v. 67 n. 17, p. 2059-2074en_HK
dc.identifier.issn0024-3205en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68281-
dc.description.abstractMelatonin inhibited thymidine incorporation into human choriocarcinoma JEG-3 cells at physiological and pharmacological concentrations in the present study. Gene expression of MT 2 receptor, but not that of mt 1 receptor, was detected in JEG-3 cells by reverse transcription-polymerase chain reaction (RT-PCR). The gene expression profile of the two human melatonin receptor subtypes in JEG-3 cells was identical to that previously reported for JAr cells, whose proliferation had also been shown to be similarly inhibited by physiological and pharmacological concentrations of melatonin. In contrast, melatonin had no effect on thymidine incorporation into 3A-Sub-E cells (a transformed trophoblast cell line), in which gene expression of both receptor subtypes could not be detected. The data suggest that in human placental trophoblasts, a correlation may exist between MT 2 receptor gene expression and the direct anti-proliferative action of melatonin. Although melatonin has been reported to induce G1/S delay in cell cycle progression of JAr cells, no significant changes in the percentages of JEG-3 cells in different cell cycle phases upon melatonin treatment was recorded by flow cytometric analysis. This indicates that G1/S transition delay is probably not an important cellular mechanism in the direct anti-proliferative action of melatonin on human JEG-3 cells in vitro. Furthermore, melatonin inhibited the growth of both JAr and JEG-3 xenograft tumors in athymic nude mice, and prolonged the survival of those animals that developed choriocarcinoma. While the number of apoptotic tumor cells was not increased by melatonin, the pineal hormone induced significant decreases in the numbers of JAr and JEG-3 cells expressing proliferating cell nuclear antigen (PCNA) and cyclin A in the tumors. Taking into account both the in vitro and in vivo findings, it is likely that the inhibitory effect of melatonin on choriocarcinoma JAr and JEG-3 cell proliferation in vivo is largely a direct action of the hormone on the tumor cells. (C) 2000 Elsevier Science Inc.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_HK
dc.relation.ispartofLife Sciencesen_HK
dc.rightsLife Sciences. Copyright © Elsevier Inc.en_HK
dc.subjectAnti-proliferationen_HK
dc.subjectChoriocarcinomaen_HK
dc.subjectCyclin Aen_HK
dc.subjectMelatoninen_HK
dc.subjectNude miceen_HK
dc.subjectPCNAen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshCell Survival - drug effectsen_HK
dc.subject.meshChoriocarcinoma - drug therapy - pathologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulation, Neoplastic - drug effects - physiologyen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMelatonin - pharmacologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshReceptors, Cell Surface - geneticsen_HK
dc.subject.meshReceptors, Cytoplasmic and Nuclear - geneticsen_HK
dc.subject.meshReceptors, Melatoninen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshUterine Neoplasms - drug therapy - pathologyen_HK
dc.subject.meshXenograft Model Antitumor Assaysen_HK
dc.titleInhibition of malignant trophoblastic cell proliferation in vitro and in vivo by melatoninen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0024-3205&volume=67&spage=2059&epage=2074&date=2000&atitle=Inhibition+of+malignant+trophoblastic+cell+proliferation+in+vitro+and+in+vivo+by+melatoninen_HK
dc.identifier.emailShiu, SYW: sywshiu@hkucc.hku.hken_HK
dc.identifier.emailYao, KM: kmyao@hku.hken_HK
dc.identifier.authorityShiu, SYW=rp00384en_HK
dc.identifier.authorityYao, KM=rp00344en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0024-3205(00)00792-Xen_HK
dc.identifier.pmid11057756-
dc.identifier.scopuseid_2-s2.0-0034665301en_HK
dc.identifier.hkuros58153en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034665301&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume67en_HK
dc.identifier.issue17en_HK
dc.identifier.spage2059en_HK
dc.identifier.epage2074en_HK
dc.identifier.isiWOS:000089476500004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridShiu, SYW=7005550655en_HK
dc.identifier.scopusauthoridXi, SC=35944696100en_HK
dc.identifier.scopusauthoridXu, JN=7407009328en_HK
dc.identifier.scopusauthoridMei, L=7103211530en_HK
dc.identifier.scopusauthoridPang, SF=7402528719en_HK
dc.identifier.scopusauthoridYao, KM=7403234578en_HK
dc.identifier.scopusauthoridWong, JTY=24467064200en_HK

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