TGF-beta and cancer

Summary

The research group's focus is on studying the dual role of transforming growth factor (TGF)-β in regulating the initiation and progression of liver cancer, as well as deciphering the relevance of other signaling pathways that interact with it, particularly the epidermal growth factor (EGF). In recent years, we have made progress in studying the TGF-β signaling pathway and have identified the production of reactive oxygen species (ROS) mediated by the NADPH oxidase family, particularly NOX4, as a key element in TGF-β function.

Currently, we are working on advancing in:

the role of TGF-β and oxidative stress in the tumor microenvironment;
identifying new targets related to TGF-β or redox stress to guide the search for novel therapeutic strategies for liver cancer;
analyzing which patients may benefit from TGF-β pathway inhibition to improve the response of hepatocellular carcinoma to immunotherapy.

268 Publications

Strategic lines

Molecular mechanisms involved in the regulation of liver regeneration, fibrosis, and cancer, with a focus on the role of TGF-β and the EGF receptor pathway in these processes.
Function of the NADPH oxidase (NOX) family as mediators of TGF-β effects. Regulation of metabolism and cellular redox balance through the TGF-β/NOX4 axis.
Tumor-stroma interaction in tumor initiation and progression: role of TGF-β in both tumor cells and the stroma. Evaluation of the therapeutic potential of TGF-β inhibitors in liver cancer.

Selected Publications

López Gil,JC;García Silva,S;Ruiz Cañas,L;Navarro,D;Palencia Campos,A;Giráldez Trujillo,A;Earl,J et al, The Peptidoglycan Recognition Protein 1 confers immune evasive properties on pancreatic cancer stem cells, Gut, 2024;73(9):1489-1508, doi:10.1136/gutjnl-2023-330995
Amengual,J;Alay,A;Vaquero,J;Gonzalez Sanchez,E;Bertran,E;Sánchez,A;Herrera,B et al, Iron chelation as a new therapeutic approach to prevent senescence and liver fibrosis progression, Cell Death Dis., 2024;15(9):680-680, doi:10.1038/s41419-024-07063-0
Gonzalez Sanchez,E;Vaquero,J;Caballero Diaz,D;Grzelak,J;Fusté,NP;Bertran,E;Amengual,J et al, The hepatocyte epidermal growth factor receptor (EGFR) pathway regulates the cellular interactome within the liver fibrotic niche, J. Pathol., 2024;263(4-5):482-495, doi:10.1002/path.6299
Ferreres,JR;Vinyals,A;Campos Martin,R;Espín,R;Podlipnik,S;Ramos,R;Bertran,E et al, PRRX1 silencing is required for metastatic outgrowth in melanoma and is an independent prognostic of reduced survival in patients, Mol. Oncol., 2024;18(10):2471-2494, doi:10.1002/1878-0261.13688
Ramos,R;Vinyals,A;Campos Martin,R;Cabré,E;Bech,JJ;Vaquero,J;Gonzalez Sanchez,E et al, New Insights into the Exosome-Induced Migration of Uveal Melanoma Cells and the Pre-Metastatic Niche Formation in the Liver, Cancers, 2024;16(17):doi:10.3390/cancers16172977

Selected Projects

PID2021-122551OB-I00. Descifrando el papel de la NADPH oxidasa NOX4 en el carcinoma hepatocelular: relevancia en células tumorales y estroma y relación con la vía del TGF-beta. Ministerio de Ciencia e Innovación. Budget: 344850. 2022-2025. PI: FABREGAT ROMERO, MARIA ISABEL.
TRANSCAN2021-237/AC22/00034. Targeting ROBOs and SLIT guidance cues in the immunosuppressive stromal context of pancreatic cancer (TRanSLIT). Instituto de Salud Carlos III (ISCIII)/ Asociación Española Contra el Cáncer (AECC). Budget: 302600. 2023-2025. PI: Espinet Hernández, Elisa Maria.
PRYGN211279FABR. Towards a precision medicine using TGF-ß inhibitors in hepatocellular carcinoma and cholangiocarcinoma. Asociación Española Contra el Cáncer (AECC). Budget: 299813,75. 2021-2025. PI: FABREGAT ROMERO, MARIA ISABEL.
PRE2022-101761. AYUDAS PARA CONTRATOS PREDOCTORALES PARA LA FORMACIÓN DE DOCTORES 2022. Ministerio de Ciencia e Innovación. Budget: 111758. 2023-2027. PI: FABREGAT ROMERO, MARIA ISABEL.
21PSJ005. Dissecting the role of the hepatocyte Epidermal Growth Factor Receptor (EGFR) pathway in the cellular interactome within the liver fibrotic niche. FUNDACIÓN RAMÓN ARECES. Budget: 112000. 2021-2024. PI: FABREGAT ROMERO, MARIA ISABEL.

Technology transfer

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