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- Scopus: eid_2-s2.0-0032532673
- PMID: 9788633
- WOS: WOS:000076455900046
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Article: Transforming growth factor β signaling through Smad1 in human breast cancer cells
Title | Transforming growth factor β signaling through Smad1 in human breast cancer cells |
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Authors | |
Issue Date | 1998 |
Publisher | American 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? |
Abstract | Previous 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 Identifier | http://hdl.handle.net/10722/171656 |
ISSN | 2023 Impact Factor: 12.5 2023 SCImago Journal Rankings: 3.468 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Liu, X | en_US |
dc.contributor.author | Yue, J | en_US |
dc.contributor.author | Frey, RS | en_US |
dc.contributor.author | Zhu, Q | en_US |
dc.contributor.author | Mulder, KM | en_US |
dc.date.accessioned | 2012-10-30T06:16:12Z | - |
dc.date.available | 2012-10-30T06:16:12Z | - |
dc.date.issued | 1998 | en_US |
dc.identifier.citation | Cancer Research, 1998, v. 58 n. 20, p. 4752-4757 | en_US |
dc.identifier.issn | 0008-5472 | en_US |
dc.identifier.uri | http://hdl.handle.net/10722/171656 | - |
dc.description.abstract | Previous 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.language | eng | en_US |
dc.publisher | American Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/ | en_US |
dc.relation.ispartof | Cancer Research | en_US |
dc.subject.mesh | Animals | en_US |
dc.subject.mesh | Bone Morphogenetic Proteins - Pharmacology | en_US |
dc.subject.mesh | Breast Neoplasms - Metabolism | en_US |
dc.subject.mesh | Dna - Biosynthesis | en_US |
dc.subject.mesh | Dna-Binding Proteins - Physiology | en_US |
dc.subject.mesh | Female | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Luciferases - Metabolism | en_US |
dc.subject.mesh | Phosphorylation | en_US |
dc.subject.mesh | Rabbits | en_US |
dc.subject.mesh | Smad Proteins | en_US |
dc.subject.mesh | Smad1 Protein | en_US |
dc.subject.mesh | Smad4 Protein | en_US |
dc.subject.mesh | Trans-Activators - Physiology | en_US |
dc.subject.mesh | Transforming Growth Factor Beta - Pharmacology | en_US |
dc.title | Transforming growth factor β signaling through Smad1 in human breast cancer cells | en_US |
dc.type | Article | en_US |
dc.identifier.email | Yue, J:jyue@hku.hk | en_US |
dc.identifier.authority | Yue, J=rp00286 | en_US |
dc.description.nature | link_to_subscribed_fulltext | en_US |
dc.identifier.pmid | 9788633 | - |
dc.identifier.scopus | eid_2-s2.0-0032532673 | en_US |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0032532673&selection=ref&src=s&origin=recordpage | en_US |
dc.identifier.volume | 58 | en_US |
dc.identifier.issue | 20 | en_US |
dc.identifier.spage | 4752 | en_US |
dc.identifier.epage | 4757 | en_US |
dc.identifier.isi | WOS:000076455900046 | - |
dc.publisher.place | United States | en_US |
dc.identifier.scopusauthorid | Liu, X=37045883900 | en_US |
dc.identifier.scopusauthorid | Yue, J=7101875828 | en_US |
dc.identifier.scopusauthorid | Frey, RS=7201607576 | en_US |
dc.identifier.scopusauthorid | Zhu, Q=7403313507 | en_US |
dc.identifier.scopusauthorid | Mulder, KM=7005187184 | en_US |
dc.identifier.issnl | 0008-5472 | - |