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Article: Transforming growth factor β signaling through Smad1 in human breast cancer cells

TitleTransforming growth factor β signaling through Smad1 in human breast cancer cells
Authors
Issue Date1998
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 1998, v. 58 n. 20, p. 4752-4757 How to Cite?
AbstractPrevious results have suggested that Smad1 transduces signals in response to bone morphogenetic proteins (BMPs), but not in response to transforming growth factor β (TGF-β). Here we investigated the ability of TGF-β to regulate Smad1 phosphorylation, hetero-oligomerization with Smad4, translocation to the nucleus, and transcriptional activation of 3TP- luciferase reporter activity in TGF-β- and BMP-responsive Hs578T human breast cancer cells. We demonstrate that Smad1 was rapidly phosphorylated in vivo in response to both TGF-β3 and BMP2 as determined using an antibody against the epitope-tagged Smad1 being expressed. In addition, both TGF-β3 and BMP2 increased Smad1-Smad4 hetero-oligomerization in Hs578T cells. Visualization of Smad1 nuclear translocation with the aid of green fluorescent protein (GFP) in live cells demonstrated nuclear accumulation of GFP-Smad1 fluorescence in response to either TGF-β or BMP2 stimulation. After ligand stimulation, approximately 60-70% of transfected cells displayed prominent nuclear fluorescence. Expression of Smad1 in Hs578T cells increased the activity of the TGF-β-responsive reporter 3TP-Lux. Moreover, TGF-β treatment further potentiated the effect of Smad1 on 3TP-luciferase activity. Collectively, our results demonstrate that TGF-β as well as BMP can signal through Smad1.
Persistent Identifierhttp://hdl.handle.net/10722/171656
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Xen_US
dc.contributor.authorYue, Jen_US
dc.contributor.authorFrey, RSen_US
dc.contributor.authorZhu, Qen_US
dc.contributor.authorMulder, KMen_US
dc.date.accessioned2012-10-30T06:16:12Z-
dc.date.available2012-10-30T06:16:12Z-
dc.date.issued1998en_US
dc.identifier.citationCancer Research, 1998, v. 58 n. 20, p. 4752-4757en_US
dc.identifier.issn0008-5472en_US
dc.identifier.urihttp://hdl.handle.net/10722/171656-
dc.description.abstractPrevious results have suggested that Smad1 transduces signals in response to bone morphogenetic proteins (BMPs), but not in response to transforming growth factor β (TGF-β). Here we investigated the ability of TGF-β to regulate Smad1 phosphorylation, hetero-oligomerization with Smad4, translocation to the nucleus, and transcriptional activation of 3TP- luciferase reporter activity in TGF-β- and BMP-responsive Hs578T human breast cancer cells. We demonstrate that Smad1 was rapidly phosphorylated in vivo in response to both TGF-β3 and BMP2 as determined using an antibody against the epitope-tagged Smad1 being expressed. In addition, both TGF-β3 and BMP2 increased Smad1-Smad4 hetero-oligomerization in Hs578T cells. Visualization of Smad1 nuclear translocation with the aid of green fluorescent protein (GFP) in live cells demonstrated nuclear accumulation of GFP-Smad1 fluorescence in response to either TGF-β or BMP2 stimulation. After ligand stimulation, approximately 60-70% of transfected cells displayed prominent nuclear fluorescence. Expression of Smad1 in Hs578T cells increased the activity of the TGF-β-responsive reporter 3TP-Lux. Moreover, TGF-β treatment further potentiated the effect of Smad1 on 3TP-luciferase activity. Collectively, our results demonstrate that TGF-β as well as BMP can signal through Smad1.en_US
dc.languageengen_US
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_US
dc.relation.ispartofCancer Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBone Morphogenetic Proteins - Pharmacologyen_US
dc.subject.meshBreast Neoplasms - Metabolismen_US
dc.subject.meshDna - Biosynthesisen_US
dc.subject.meshDna-Binding Proteins - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshHumansen_US
dc.subject.meshLuciferases - Metabolismen_US
dc.subject.meshPhosphorylationen_US
dc.subject.meshRabbitsen_US
dc.subject.meshSmad Proteinsen_US
dc.subject.meshSmad1 Proteinen_US
dc.subject.meshSmad4 Proteinen_US
dc.subject.meshTrans-Activators - Physiologyen_US
dc.subject.meshTransforming Growth Factor Beta - Pharmacologyen_US
dc.titleTransforming growth factor β signaling through Smad1 in human breast cancer cellsen_US
dc.typeArticleen_US
dc.identifier.emailYue, J:jyue@hku.hken_US
dc.identifier.authorityYue, J=rp00286en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid9788633-
dc.identifier.scopuseid_2-s2.0-0032532673en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0032532673&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume58en_US
dc.identifier.issue20en_US
dc.identifier.spage4752en_US
dc.identifier.epage4757en_US
dc.identifier.isiWOS:000076455900046-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLiu, X=37045883900en_US
dc.identifier.scopusauthoridYue, J=7101875828en_US
dc.identifier.scopusauthoridFrey, RS=7201607576en_US
dc.identifier.scopusauthoridZhu, Q=7403313507en_US
dc.identifier.scopusauthoridMulder, KM=7005187184en_US

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