The Snail gene family of transcription factors plays important roles during embryonic development in processes that imply profound cell movements. These functions are essentially mediated by the triggering of the epithelial-mesenchymal transition (EMT), a phenotypic change that renders epithelial cells migratory and invasive. EMT is also a well-known process that occurs in the acquisition of invasive and migratory properties during tumour progression. Indeed, Snail genes have been coopted for the acquisition of malignant properties in epithelial tumours. It is well known that EMT can be triggered by different growth factors, including FGF, TGF-beta, HGF, etc. and recent results from several laboratories including the host lab indicate that all of them induce Snail expression concomitant with the induction of EMT. Thus, Snail may be a point of convergence of the signalling pathways triggered by these growth factors, and thus, located at the crossroads of the EMT.
Interestingly, unpublished data from the host l ab indicate that Snail also protects from cell death, leading to the idea that the process of EMT may be associated to cell survival through Snail. This link is of high interest due to the fact that tumour cells are indeed more resistant to cell death than their normal counterparts. The aim of my postdoctoral period in the team of Angela Nieto is to check the hypothesis of Snail being a central point during the triggering of EMT both in physiology and pathology. I will take advantage of my previous knowledge in Cell Biology and in the culture of cells and organs and particularly, of my background in the analysis of cell death both in vitro and in vivo. In addition to analyse the effects of growth factors on epithelial cells regarding the induction of EMT and Snail, I will use different cell lines with constitutive or inducible Snail expression, RNA interference strategies and a mouse transgenic model generated in the host lab with inducible Snail expression.
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