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TGF-β Signaling in Immunity, Inflammation, Fibrosis and Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 20 November 2025 | Viewed by 2655

Special Issue Editors


E-Mail Website1 Website2
Guest Editor
1. TGF-β and Cancer Group, Oncobell Program, Bellvitge Biomedical Research Institute (IDIBELL), Gran Via de l'Hospitalet, 199, L'Hospitalet de Llobregat, 08908 Barcelona, Spain
2. Oncology Program, CIBEREHD, Instituto de Salud Carlos III, 28029 Madrid, Spain
Interests: TGF-beta; EGF; NADPH oxidases; NOX4; oxidative stress; epithelial–mesenchymal transition (EMT); liver stem cells; metabolism and liver; liver cancer; HCC; liver fibrosis; liver signaling
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Scientific Direction, National Institute of Gastroenterology “S. de Bellis”, IRCCS Research Hospital, Via Turi 27, Castellana Grotte, 70013 Bari, Italy
Interests: HCC; CCA; tumor microenvironment; cancer therapy; biomarkers; TGF-beta
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The transforming growth factor-beta (TGF-β) family plays essential roles in the regulation of different cellular processes that are essential for the homeostasis of tissues and organs. Because of the diverse and pleiotropic TGF-β functions, dysregulation of TGF-β family signaling can lead to a plethora of developmental disorders and diseases.

Due to its role in immune homeostasis, perturbations of TGF-β signaling underlies inflammatory diseases. Many chronic inflammatory diseases are marked by fibrosis, which concurs with excessive deposition of the extracellular matrix, resulting in the loss of normal function of the affected organs. The TGF-β family also plays essential roles in the initiation and progression of fibrosis, through the activation of fibroblasts towards a myofibroblast phenotype. During the early stages of tumorigenesis, TGF-β may act as a tumor suppressor by inducing cytostasis and apoptosis of preneoplastic cells. However, at later stages, when cancer cells have acquired oncogenic mutations that allow scaping from TGF-β tumor suppressor function, it becomes a tumor promoter by stimulating tumor cells to undergo epithelial–mesenchymal Transition (EMT), which increases migration and invasion.  TGF-β is also central to immune suppression within the tumor microenvironment, and recent studies have revealed roles in tumor immune evasion and poor responses to cancer immunotherapy.

In this Special Issue, we invite contributions that, in the form of original articles or reviews, will help to clarify the complex role of the TGF-β family in human diseases.

Dr. Isabel Fabregat
Prof. Dr. Gianluigi Giannelli
Guest Editors

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Keywords

  • TGF-beta
  • fibrosis
  • inflammation
  • cancer
  • immune cells
  • fibroblasts
  • EMT
  • immunotherapy

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Published Papers (1 paper)

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Research

16 pages, 6246 KiB  
Article
New Hepatocellular Carcinoma (HCC) Primary Cell Cultures as Models for Exploring Personalized Anti-TGF-β Therapies Based on Tumor Characteristics
by Rosanna Scialpi, Rut Espinosa-Sotelo, Esther Bertran, Francesco Dituri, Gianluigi Giannelli and Isabel Fabregat
Int. J. Mol. Sci. 2025, 26(6), 2430; https://doi.org/10.3390/ijms26062430 - 8 Mar 2025
Viewed by 2055
Abstract
Transforming growth factor-beta (TGF-β) plays a dual role in hepatocellular carcinoma (HCC), acting as a tumor suppressor in early stages by inducing cell cycle arrest and apoptosis, and as a promoter in advanced stages by fostering tumor progression, epithelial–mesenchymal transition (EMT), and metastasis. [...] Read more.
Transforming growth factor-beta (TGF-β) plays a dual role in hepatocellular carcinoma (HCC), acting as a tumor suppressor in early stages by inducing cell cycle arrest and apoptosis, and as a promoter in advanced stages by fostering tumor progression, epithelial–mesenchymal transition (EMT), and metastasis. Understanding TGF-β’s role in HCC progression, particularly its impact on tumor–stroma interactions, is crucial for developing personalized therapies. This study aims to clarify TGF-β function in HCC using patient-derived cell lines and advanced 2D and 3D culture models. Three new cell lines (HLC21, HLC19 tumoral, and HLC19 metastatic) were isolated from HCC patient biopsies, characterizing their phenotypic markers and responses to TGF-β and its inhibitor, galunisertib. HLC21 cells displayed a mixed epithelial–mesenchymal phenotype, responding to TGF-β suppressing growth and undergoing EMT, which were inhibited by galunisertib. Conversely, HLC19 tumoral and metastatic cells exhibited mesenchymal phenotypes and were resistant to both TGF-β suppression and galunisertib effects. In 3D co-cultures with hepatic fibroblasts, TGF-β inhibitory effects were diminished for responsive cell lines, while resistant lines maintained their non-responsiveness. These findings highlight TGF-β’s dual role in HCC and its influence on tumor–stroma crosstalk, offering valuable models for exploring personalized anti-TGF-β therapies based on tumor characteristics. Full article
(This article belongs to the Special Issue TGF-β Signaling in Immunity, Inflammation, Fibrosis and Cancer)
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