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Updated: Jul 14, 2026

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
Published on: October 27, 2020
TGF-beta modulates beta-Catenin stability and signaling in mesenchymal proliferations
Saeid Amini Nik1, Rasoul Pour Ebrahim, Kim Van Dam
1Department of Human Genetics, Catholic University of Leuven, Herestraat 49, Leuven, Belgium.
Abstract:
Here for the first time we showed, despite the oncogenic mutations in beta-Catenin, that TGF-beta is a modulator of beta-Catenin levels in tumoral fibroblasts as well as non-tumoral fibroblasts. The results show that the TGF-beta pathway is active in desmoids cells and in in situ tumors. A dose dependent increase in beta-Catenin protein levels was observed after TGF-beta treatment in combination with an increased repression of GSK-3beta both in normal and tumoral fibroblasts. TGF-beta stimulation also led to an altered -- up to 5 fold -- transcriptional activity of beta-Catenin responsive promoters, such as IGFBP6 as well as increase of TOPflash activity. TGF-beta stimulation increased cell proliferation and BrdU incorporation 2.5 times. Taken together, we propose that TGF-beta is a modulator of beta-Catenin levels in tumoral fibroblasts and non-tumoral fibroblasts, despite the oncogenic mutations already present in this gene in tumoral fibroblasts of desmoid tumors. This modulation of beta-Catenin levels by TGF-beta may be involved in determining the tumoral phenotype of the cells.
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