SMAD1/5 AND CANCER
A novel mode of TGF-beta signalling through Smad1/Smad5 phosphorylation: mechanism and functional role in cancer
| Coordinatore | CANCER RESEARCH UK
Organization address
address: ST JOHN STREET 407 ANGEL BUILDING contact info |
| Nazionalità Coordinatore | United Kingdom [UK] |
| Totale costo | 171˙867 € |
| EC contributo | 171˙867 € |
| Programma | FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013) |
| Code Call | FP7-PEOPLE-IEF-2008 |
| Funding Scheme | MC-IEF |
| Anno di inizio | 2009 |
| Periodo (anno-mese-giorno) | 2009-05-27 - 2011-05-26 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
CANCER RESEARCH UK
Organization address
address: ST JOHN STREET 407 ANGEL BUILDING contact info |
UK (LONDON) | coordinator | 171˙867.62 |
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Obiettivo del progetto (Objective)
'Ligands of the Transfroming Growth Factor-beta (TGF-beta) superfamily control numerous cellular processes such as proliferation, apoptosis, differentiation, adhesion and mobility. As a result, it is well established that they play an essential role in cancer. TGF-beta signalling has been implicated in both tumour suppression and progression. TGF-beta signals predominantly through receptor-regulated Smads (R-Smads), Smad2 and Smad3, but several lines of evidence from the Hill’s lab suggest that TGF-beta can also strongly induce phosphorylation and consequently signalling by Smad1 and Smad5 in epithelial cells. Moreover, our recent results have shown that Smad1/5 activation by TGF-beta is not required for its growth inhibitory effects, but rather is specifically required for TGF-beta-induced anchorage-independent growth, suggesting a relevant role of this novel mode of signalling in tumor progression. The first aim of this project is the accurate molecular description of TGF-beta-induced activation of Smad1/5. We will focus both on the receptor complexes responsible and the types of Smad complexes that result. Then, we will study which genes are induced by this novel mode of TGF-beta signalling. Finally, its functional relevance in normal epithelial cells and in tumorigenesis will be assessed. If we can show that this novel branch of TGF-beta signalling plays a role in tumour growth, then it could provide a good therapeutic target in cancer.'