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688164.pdf (2.21 MB)

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Data de publicació

2018-09-10

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cc-by (c) Fabregat Romero, Isabel et al., 2018
Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/141529

Transforming growth factor-β-induced cell plasticity in liver fibrosis and hepatocarcinogenesis

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Recurs relacionat

https://doi.org/10.3389/fonc.2018.00357

Resum

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.

Matèries

Càncer, Cèl·lules hepàtiques, Fetge, Plasticitat

Matèries (anglès)

Cancer, Liver cells, Liver, Plasticity

Citació

Col·leccions

Articles publicats en revistes (Ciències Fisiològiques)
Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))

Citació

FABREGAT ROMERO, Isabel and CABALLERO DÍAZ, Daniel. Transforming growth factor-β-induced cell plasticity in liver fibrosis and hepatocarcinogenesis. Frontiers in Oncology. 2018. Vol. 8, num. 357. ISSN 2234-943X. [consulted: 13 of August of 2026]. Available at: https://hdl.handle.net/2445/141529

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