Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/141529
Title: Transforming growth factor-β-induced cell plasticity in liver fibrosis and hepatocarcinogenesis
Author: Fabregat Romero, Isabel
Caballero-Diaz, Daniel
Keywords: Càncer
Cèl·lules hepàtiques
Fetge
Plasticitat
Cancer
Liver cells
Liver
Plasticity
Issue Date: 10-Sep-2018
Publisher: Frontiers Media
Abstract: The Transforming Growth Factor-beta (TGF-β) family plays relevant roles in the regulation of different cellular processes that are essential for tissue and organ homeostasis. In the case of the liver, TGF-β signaling participates in different stages of disease progression, from initial liver injury toward fibrosis, cirrhosis and cancer. When a chronic injury takes place, mobilization of lymphocytes and other inflammatory cells occur, thus setting the stage for persistence of an inflammatory response. Macrophages produce profibrotic mediators, among them, TGF-β, which is responsible for activation -transdifferentiation- of quiescent hepatic stellate cells (HSC) to a myofibroblast (MFB) phenotype. MFBs are the principal source of extracellular matrix protein (ECM) accumulation and prominent mediators of fibrogenesis. TGF-β also mediates an epithelial-mesenchymal transition (EMT) process in hepatocytes that may contribute, directly or indirectly, to increase the MFB population. In hepatocarcinogenesis, TGF-β plays a dual role, behaving as a suppressor factor at early stages, but contributing to later tumor progression, once cells escape from its cytostatic effects. As part of its potential pro-tumorigenic actions, TGF-β induces EMT in liver tumor cells, which increases its pro-migratory and invasive potential. In parallel, TGF-β also induces changes in tumor cell plasticity, conferring properties of a migratory tumor initiating cell (TIC). The main aim of this review is to shed light about the pleiotropic actions of TGF-β that explain its effects on the different liver cell populations. The cross-talk with other signaling pathways that contribute to TGF-β effects, in particular the Epidermal Growth Factor Receptor (EGFR), will be presented. Finally, we will discuss the rationale for targeting the TGF-β pathway in liver pathologies.
Note: Reproducció del document publicat a: https://doi.org/10.3389/fonc.2018.00357
It is part of: Frontiers in Oncology, 2018, vol. 8, p. 357
URI: http://hdl.handle.net/2445/141529
Related resource: https://doi.org/10.3389/fonc.2018.00357
ISSN: 2234-943X
Appears in Collections:Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))
Articles publicats en revistes (Ciències Fisiològiques)

Files in This Item:
File Description SizeFormat 
688164.pdf2.26 MBAdobe PDFView/Open


This item is licensed under a Creative Commons License Creative Commons