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

Carla Cicchini, Ilaria Laudadio, Franca Citarella, Marco Corazzari, Corinna Steindler, Alice Conigliaro, Antonio Fantoni, Laura Amicone, Marco Tripodi

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)143-152
Number of pages10
JournalExperimental Cell Research
Issue number1
Publication statusPublished - Jan 1 2008


  • FAK
  • MT
  • Src
  • TGFβ

ASJC Scopus subject areas

  • Cell Biology


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