Salta al contenuto principale
Passa alla visualizzazione normale.


TGFβ-induced EMT requires focal adhesion kinase (FAK) signaling

  • Autori: Cicchini, C.; Laudadio, I.; Citarella, F.; Corazzari, M.; Steindler, C.; Conigliaro, A.; Fantoni, A.; Amicone, L.; Tripodi, M.
  • Anno di pubblicazione: 2008
  • Tipologia: Articolo in rivista (Articolo in rivista)
  • Parole Chiave: FAK; MT; Src; TGFβ; Animals; Biomarkers, Tumor; Cadherins; Cell Line; Cell Transformation, Neoplastic; Enzyme Activation; Epithelial Cells; Focal Adhesion Protein-Tyrosine Kinases; Hepatocytes; Liver Neoplasms; Mesoderm; Mice; Neoplasm Invasiveness; Signal Transduction; Transcriptional Activation; Transforming Growth Factor beta; Up-Regulation; src-Family Kinases; Cell Biology
  • OA Link:


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 TGFβ induces a full EMT characterized by (i) Snail induction, (ii) E-cadherin delocalization and down-regulation, (iii) down-regulation of the hepatocyte transcriptional factor HNF4α 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 TGFβ 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 TGFβ-mediated EMT in hepatocytes. © 2007 Elsevier Inc. All rights reserved.