A5042151289- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Nitric Oxide and Endothelin Effects
- Cancer, Hypoxia, and Metabolism
- Immune cells in cancer
- Cell Adhesion Molecules Research
- Phagocytosis and Immune Regulation
- Metabolism, Diabetes, and Cancer
- Adenosine and Purinergic Signaling
- Cancer, Lipids, and Metabolism
- Redox biology and oxidative stress
- Inflammatory mediators and NSAID effects
- Diet and metabolism studies
- TGF-β signaling in diseases
- Histone Deacetylase Inhibitors Research
- Axon Guidance and Neuronal Signaling
- Macrophage Migration Inhibitory Factor
- Caveolin-1 and cellular processes
- Signaling Pathways in Disease
- Epigenetics and DNA Methylation
- Liver physiology and pathology
- Cancer Mechanisms and Therapy
- Protein Degradation and Inhibitors
Institut d'Investigació Biomédica de Bellvitge
2017-2024
Instituto de Salud Carlos III
2019-2024
Bellvitge University Hospital
2021-2024
Centro de Investigación Biomédica en Red
2022-2023
Universitat de Barcelona
2023
Centro de Investigación Biomédica en Red de Enfermedades Hepáticas y Digestivas
2021
Abstract Transforming Growth Factor beta (TGF-β) induces tumor cell migration and invasion. However, its role in inducing metabolic reprogramming is poorly understood. Here we analyzed the profile of hepatocellular carcinoma (HCC) cells that show differences TGF-β expression. Oxygen consumption rate (OCR), extracellular acidification (ECAR), metabolomics transcriptomics were performed. Results indicated switch from an epithelial to a mesenchymal/migratory phenotype HCC characterized by...
(1) Background: The transforming growth factor (TGF)-β plays a dual role in liver carcinogenesis. At early stages, it inhibits cell and induces apoptosis. However, TGF-β expression is high advanced stages of hepatocellular carcinoma (HCC) cells become resistant to induced suppressor effects, responding this cytokine undergoing epithelial–mesenchymal transition (EMT), which contributes migration invasion. Metabolic reprogramming has been established as key hallmark cancer. consider metabolism...
The NADPH oxidase NOX4 plays a tumor-suppressor function in HCC. Silencing confers higher proliferative and migratory capacity to HCC cells increases their vivo tumorigenic potential xenografts mice. gene deletions are frequent HCC, correlating with tumor grade worse recurrence-free overall survival rates. However, despite the accumulating evidence of protective regulatory role cellular processes governed by not yet understood. Accordingly, aim this work was better understand molecular...
Upon ligand binding, tyrosine kinase receptors, such as epidermal growth factor receptor (EGFR), are recruited into clathrin-coated pits for internalization by endocytosis, which is relevant signalling and/or degradation. In liver cells, transforming factor-β (TGF-β) induces both pro- and anti-apoptotic signals; the latter mediated EGFR pathway. Since mainly traffics via vesicles, we aimed to analyse potential role of clathrin in TGF-β-induced cells its relevance cancer.Real-Time PCR...
// Jitka Soukupova 1 , Esther Bertran Irene Peñuelas-Haro Uxue Urdiroz-Urricelqui 1, 2 Matthias Borgman 3 Hella Kohlhof 3, 4 and Isabel Fabregat "TGF-β cancer" group, Oncobell Program. Bellvitge Biomedical Research Institute, (IDIBELL), L´Hospitalet, Barcelona, Spain Department of Physiological Sciences, Faculty Medicine Health Sciences. University Barcelona (UB), 4SC AG, Planegg-Martinsried, Germany Immunic Correspondence to: Fabregat, email: ifabregat@idibell.cat Keywords: HDAC inhibitors;...
The NADPH oxidase NOX4 has been proposed as necessary for the apoptosis induced by Transforming Growth Factor-beta (TGF-β) in hepatocytes and hepatocellular carcinoma (HCC) cells. However, whether is required TGF-β-induced canonical (SMADs) or non-canonical signals not fully understood yet, neither its potential involvement other parallel actions TGF-β. In this work we have used CRISPR Cas9 technology to stable attenuate expression HCC Results indicated that an efficient SMAD2/3...
How pancreatic cancer cells acquire tumor initiating capacities remains poorly understood. A recent study by Yamazaki et al (2023) uncovers a crucial, targetable role of tyrosine kinase‐like orphan receptor (ROR1) in PDAC formation and progression.