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http://hdl.handle.net/2445/141529
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DC Field | Value | Language |
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dc.contributor.author | Fabregat Romero, Isabel | - |
dc.contributor.author | Caballero Díaz, Daniel | - |
dc.date.accessioned | 2019-10-02T15:55:17Z | - |
dc.date.available | 2019-10-02T15:55:17Z | - |
dc.date.issued | 2018-09-10 | - |
dc.identifier.issn | 2234-943X | - |
dc.identifier.uri | http://hdl.handle.net/2445/141529 | - |
dc.description.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. | - |
dc.format.extent | 18 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Frontiers Media | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.3389/fonc.2018.00357 | - |
dc.relation.ispartof | Frontiers in Oncology, 2018, vol. 8, p. 357 | - |
dc.relation.uri | https://doi.org/10.3389/fonc.2018.00357 | - |
dc.rights | cc-by (c) Fabregat Romero, Isabel et al., 2018 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es | - |
dc.source | Articles publicats en revistes (Ciències Fisiològiques) | - |
dc.subject.classification | Càncer | - |
dc.subject.classification | Cèl·lules hepàtiques | - |
dc.subject.classification | Fetge | - |
dc.subject.classification | Plasticitat | - |
dc.subject.other | Cancer | - |
dc.subject.other | Liver cells | - |
dc.subject.other | Liver | - |
dc.subject.other | Plasticity | - |
dc.title | Transforming growth factor-β-induced cell plasticity in liver fibrosis and hepatocarcinogenesis | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.identifier.idgrec | 688164 | - |
dc.date.updated | 2019-10-02T15:55:17Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 30250825 | - |
Appears in Collections: | Articles publicats en revistes (Ciències Fisiològiques) Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
Files in This Item:
File | Description | Size | Format | |
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688164.pdf | 2.26 MB | Adobe PDF | View/Open |
This item is licensed under a Creative Commons License