Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10904747 | Experimental Cell Research | 2007 | 9 Pages |
Abstract
Here for the first time we showed, despite the oncogenic mutations in β-Catenin, that TGF-β is a modulator of β-Catenin levels in tumoral fibroblasts as well as non-tumoral fibroblasts. The results show that the TGF-β pathway is active in desmoids cells and in in situ tumors. A dose dependent increase in β-Catenin protein levels was observed after TGF-β treatment in combination with an increased repression of GSK-3β both in normal and tumoral fibroblasts. TGF-β stimulation also led to an altered - up to 5 fold - transcriptional activity of β-Catenin responsive promoters, such as IGFBP6 as well as increase of TOPflash activity. TGF-β stimulation increased cell proliferation and BrdU incorporation 2.5 times. Taken together, we propose that TGF-β is a modulator of β-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 β-Catenin levels by TGF-β may be involved in determining the tumoral phenotype of the cells.
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Authors
Saeid Amini Nik, Rasoul Pour Ebrahim, Kim Van Dam, Jean-Jacques Cassiman, Sabine Tejpar,