Journal
EXPERIMENTAL CELL RESEARCH
Volume 314, Issue 1, Pages 143-152Publisher
ELSEVIER INC
DOI: 10.1016/j.yexcr.2007.09.005
Keywords
MT; TGF beta; FAK; Src
Categories
Funding
- Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom
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The epithelial-to-mesenchymal transition (EMT) is a crucial process, occurring both during development and tumor progression, by which an epithelial cell undergoes a conversion to a mesenchymal phenotype, dissociates from initial contacts and migrates to secondary sites. We recently reported that in hepatocytes the multifunctional cytokine TGF beta induces a full EMT characterized by (i) Snail induction, (ii) E-cadherin delocalization and down-regulation, (iii) down-regulation of the hepatocyte transcriptional factor HNF4 alpha and (iv) up-regulation of mesenchymal and invasiveness markers. In particular, we showed that Snail directly causes the transcriptional down-regulation of E-cadherin and HNF4, while it is not sufficient for the up-regulation of mesenchymal and invasiveness EMT markers. In this paper, we show that in hepatocytes TGF beta, induces a Src-dependent activation of the focal adhesion protein FAK. More relevantly, we gathered results indicating that FAK signaling is required for (i) transcriptional up-regulation of mesenchymal and invasiveness markers and (ii) delocalization of membrane-bound E-cadherin. Our results provide the first evidence of FAK functional role in TGF beta-mediated EMT in hepatocytes. (C) 2007 Elsevier Inc. All rights reserved.
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