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

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

Risultato della ricerca: Articlepeer review

187 Citazioni (Scopus)

Abstract

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.
Lingua originaleEnglish
pagine (da-a)143-152
Numero di pagine10
RivistaExperimental Cell Research
Volume314
Stato di pubblicazionePublished - 2008

All Science Journal Classification (ASJC) codes

  • Cell Biology

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