Antagonistic regulation of EMT by TIF1g and Smad4 in mammary epithelial cells
نویسندگان
چکیده
TGF-b is a potent inducer of epithelial-to-mesenchymal transition (EMT), a process involved in tumour invasion. TIF1c participates in TGF-b signalling. To understand the role of TIF1c in TGF-b signalling and its requirement for EMT, we analysed the TGF-b1 response of human mammary epithelial cell lines. A strong EMT increase was observed in TIF1c-silenced cells after TGF-b1 treatment, whereas Smad4 inactivation completely blocked this process. Accordingly, the functions of several TIF1c target genes can be linked to EMT, as shown by microarray analysis. As a negative regulator of Smad4, TIF1c could be crucial for the regulation of TGF-b signalling. Furthermore, TIF1c binds to and represses the plasminogen activator inhibitor 1 promoter, demonstrating a direct role of TIF1c in TGF-b-dependent gene expression. This study shows the molecular relationship between TIF1c and Smad4 in TGF-b signalling and EMT.
منابع مشابه
Antagonistic regulation of EMT by TIF1γ and Smad4 in mammary epithelial cells.
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