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Article: Adiponectin modulates the glycogen synthase kinase-3β/β-catenin signaling pathway and attenuates mammary tumorigenesis of MDA-MB-231 cells in nude mice

TitleAdiponectin modulates the glycogen synthase kinase-3β/β-catenin signaling pathway and attenuates mammary tumorigenesis of MDA-MB-231 cells in nude mice
Authors
KeywordsChemicals And Cas Registry Numbers
Issue Date2006
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2006, v. 66 n. 23, p. 11462-11470 How to Cite?
AbstractAdiponectin is an adipokine that has pleiotropic beneficial roles in systemic insulin resistance and inflammation. Several recent clinical studies suggest that low serum levels of adiponectin are associated with increased risks of breast cancer. Here, we investigated the direct effects of adiponectin on breast cancer development in vitro and in vivo. Our results showed that adiponectin significantly attenuated the proliferations of two typical human breast cancer cells, MDA-MB-231 and T47D, in a cell type-specific manner. Further analysis revealed that adiponectin could induce apoptosis and arrest the cell cycle progression at G0-G1 phase in MDA-MB-231 cells. Prolonged treatment with adiponectin in this cell line blocked serum-induced phosphorylation of Akt and glycogen synthase kinase-3β (GSK-3β), suppressed intracellular accumulation of β-catenin and its nuclear activities, and consequently reduced expression of cyclin D1. Adiponectin-mediated suppression of cyclin D1 expression and attenuation of cell proliferation was abrogated by the GSK-3β inhibitor lithium chloride. These results suggest that the inhibitory role of adiponectin on MDA-MB-231 cell growth might be attributed to its suppressive effects on the GSK-3β/β-catenin signaling pathway. Furthermore, our in vivo study showed that both supplementation of recombinant adiponectin and adenovirus-mediated overexpression of this adipokine substantially reduced the mammary tumorigenesis of MDA-MB-231 cells in female nude mice. Taken together, these data support the role of adiponectin as a negative regulator of breast cancer development and also suggest that adiponectin might represent a novel therapeutic target for this disease. ©2006 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/91503
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Yen_HK
dc.contributor.authorLam, JBen_HK
dc.contributor.authorLam, KSLen_HK
dc.contributor.authorLiu, Jen_HK
dc.contributor.authorLam, MCen_HK
dc.contributor.authorHoo, RLCen_HK
dc.contributor.authorWu, Den_HK
dc.contributor.authorCooper, GJSen_HK
dc.contributor.authorXu, Aen_HK
dc.date.accessioned2010-09-17T10:20:27Z-
dc.date.available2010-09-17T10:20:27Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer Research, 2006, v. 66 n. 23, p. 11462-11470en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/91503-
dc.description.abstractAdiponectin is an adipokine that has pleiotropic beneficial roles in systemic insulin resistance and inflammation. Several recent clinical studies suggest that low serum levels of adiponectin are associated with increased risks of breast cancer. Here, we investigated the direct effects of adiponectin on breast cancer development in vitro and in vivo. Our results showed that adiponectin significantly attenuated the proliferations of two typical human breast cancer cells, MDA-MB-231 and T47D, in a cell type-specific manner. Further analysis revealed that adiponectin could induce apoptosis and arrest the cell cycle progression at G0-G1 phase in MDA-MB-231 cells. Prolonged treatment with adiponectin in this cell line blocked serum-induced phosphorylation of Akt and glycogen synthase kinase-3β (GSK-3β), suppressed intracellular accumulation of β-catenin and its nuclear activities, and consequently reduced expression of cyclin D1. Adiponectin-mediated suppression of cyclin D1 expression and attenuation of cell proliferation was abrogated by the GSK-3β inhibitor lithium chloride. These results suggest that the inhibitory role of adiponectin on MDA-MB-231 cell growth might be attributed to its suppressive effects on the GSK-3β/β-catenin signaling pathway. Furthermore, our in vivo study showed that both supplementation of recombinant adiponectin and adenovirus-mediated overexpression of this adipokine substantially reduced the mammary tumorigenesis of MDA-MB-231 cells in female nude mice. Taken together, these data support the role of adiponectin as a negative regulator of breast cancer development and also suggest that adiponectin might represent a novel therapeutic target for this disease. ©2006 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subjectChemicals And Cas Registry Numbersen_HK
dc.subject.meshActive Transport, Cell Nucleus - drug effectsen_HK
dc.subject.meshAdiponectin - genetics - pharmacologyen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshBreast Neoplasms - metabolism - pathology - therapyen_HK
dc.subject.meshCattleen_HK
dc.subject.meshCell Cycle - drug effectsen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Movement - drug effectsen_HK
dc.subject.meshCell Nucleus - drug effects - metabolismen_HK
dc.subject.meshCell Proliferation - drug effectsen_HK
dc.subject.meshCulture Media - chemistry - pharmacologyen_HK
dc.subject.meshCyclin D1 - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFetal Blooden_HK
dc.subject.meshGene Therapy - methodsen_HK
dc.subject.meshGlycogen Synthase Kinase 3 - antagonists & inhibitors - metabolismen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshPhosphorylation - drug effectsen_HK
dc.subject.meshProto-Oncogene Proteins c-akt - metabolismen_HK
dc.subject.meshSignal Transduction - drug effectsen_HK
dc.subject.meshXenograft Model Antitumor Assays - methodsen_HK
dc.subject.meshbeta Catenin - metabolismen_HK
dc.titleAdiponectin modulates the glycogen synthase kinase-3β/β-catenin signaling pathway and attenuates mammary tumorigenesis of MDA-MB-231 cells in nude miceen_HK
dc.typeArticleen_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.emailLam, KSL: ksllam@hku.hken_HK
dc.identifier.emailHoo, RLC: rubyhoo@hkucc.hku.hken_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.identifier.authorityLam, KSL=rp00343en_HK
dc.identifier.authorityHoo, RLC=rp01334en_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1158/0008-5472.CAN-06-1969en_HK
dc.identifier.pmid17145894-
dc.identifier.scopuseid_2-s2.0-33845806853en_HK
dc.identifier.hkuros126076-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33845806853&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume66en_HK
dc.identifier.issue23en_HK
dc.identifier.spage11462en_HK
dc.identifier.epage11470en_HK
dc.identifier.isiWOS:000242614300050-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridLam, JB=26653294900en_HK
dc.identifier.scopusauthoridLam, KSL=8082870600en_HK
dc.identifier.scopusauthoridLiu, J=36066808300en_HK
dc.identifier.scopusauthoridLam, MC=36879143100en_HK
dc.identifier.scopusauthoridHoo, RLC=6602369766en_HK
dc.identifier.scopusauthoridWu, D=7404297751en_HK
dc.identifier.scopusauthoridCooper, GJS=7402355946en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK

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