A5045576510- Epigenetics and DNA Methylation
- Lung Cancer Treatments and Mutations
- Peptidase Inhibition and Analysis
- Metastasis and carcinoma case studies
- Cancer-related gene regulation
- Mechanisms of cancer metastasis
- Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
- Protease and Inhibitor Mechanisms
- Fibroblast Growth Factor Research
- Occupational and environmental lung diseases
- Cancer, Hypoxia, and Metabolism
- Ferroptosis and cancer prognosis
- Pulmonary Hypertension Research and Treatments
- Angiogenesis and VEGF in Cancer
- Histone Deacetylase Inhibitors Research
- Immune cells in cancer
- Lung Cancer Research Studies
- Hepatocellular Carcinoma Treatment and Prognosis
- 3D Printing in Biomedical Research
- Tissue Engineering and Regenerative Medicine
- Cancer Cells and Metastasis
- Medical Imaging and Pathology Studies
- Cardiac Fibrosis and Remodeling
- Cellular Mechanics and Interactions
- Proteoglycans and glycosaminoglycans research
Universitat de Barcelona
2017-2024
FC Barcelona
2019
Idiopathic pulmonary fibrosis (IPF) is an aggressive disease in which normal lung parenchyma replaced by a stiff dysfunctional scar rich activated fibroblasts and collagen-I. We examined how the mechanochemical pro-fibrotic microenvironment provided matrix stiffening TGF-β1 cooperates transcriptional control of collagen homeostasis fibrotic conditions. For this purpose we cultured from IPF patients or donors on hydrogels with tunable elasticity, including 3D collagen-I gels 2D polyacrylamide...
Large cell carcinoma (LCC) is a rare and aggressive lung cancer subtype with poor prognosis no targeted therapies. Tumor-associated fibroblasts (TAFs) derived from LCC tumors exhibit premature senescence, coculture of pulmonary lines selectively induces fibroblast which in turn drives growth invasion. Here we identify MMP1 as overexpressed specifically lines, show that expression by cells necessary for induction senescence consequent tumor promotion both culture mouse models. We also MMP1,...
Tissue inhibitor of metalloproteinase-1 (TIMP-1) is an important regulator extracellular matrix turnover that has been traditionally regarded as a potential tumor suppressor owing to its inhibitory effects metalloproteinases. Intriguingly, this interpretation challenged by the consistent observation increased expression TIMP-1 associated with poor prognosis in virtually all cancer types including lung cancer, supporting tumor-promoting function. However, how dysregulated within...
The contribution of epithelial-to-mesenchymal transition (EMT) to the profibrotic stiff microenvironment and myofibroblast accumulation in pulmonary fibrosis remains unclear. We examined EMT-competent lung epithelial cells fibroblasts from control (fibrosis-free) donors or patients with idiopathic (IPF), which is a very aggressive fibrotic disorder. Cells were cultured on conditions including substrata TGF-β1, analyzed terms morphology, stiffness, expression EMT/myofibroblast markers...
Abstract The tumor-promoting fibrotic stroma rich in tumor-associated fibroblasts (TAF) is drawing increased therapeutic attention. Intriguingly, a trial with the antifibrotic drug nintedanib non–small cell lung cancer reported clinical benefits adenocarcinoma (ADC) but not squamous carcinoma (SCC), even though both histotypes. Likewise, we that inhibited phenotype of TAFs selectively ADC. Here show tumor fibrosis actually higher ADC-TAFs than SCC-TAFs vitro and patient samples....
Myofibroblasts are a population of highly contractile fibroblasts that express and require the activity transcription factor Snail1. Cancer-associated (CAFs) correlate with low survival cancer patients when present in stroma primary tumors. Remarkably, presence myofibroblastic CAFs (which Snail1) creates mechanical properties tumor microenvironment support metastasis. However, therapeutic blockage fibroblast is double-edged sword, as normal activities often restrict cell invasion. We used...
Abstract The fibrotic tumor microenvironment is a pivotal therapeutic target. Nintedanib, clinically approved multikinase antifibrotic inhibitor, effective against lung adenocarcinoma (ADC) but not squamous cell carcinoma (SCC). Previous studies have implicated the secretome of tumor‐associated fibroblasts (TAFs) in selective effects nintedanib ADC, driving factor(s) remained unidentified. Here we examined role tissue inhibitor metalloproteinase‐1 (TIMP‐1), tumor‐promoting cytokine...
The 16th ERS Lung Science Conference (LSC) took place on March 8–11, 2018, in Estoril, Portugal, with around 200 delegates from all over the world. This year's topic was "Cell-matrix interactions lung disease and regeneration" involved excellent presentations by leading experts field covering everything exploratory studies how matrix functions, remodelling biomarkers disease, to more technical knowledge described of bioengineering. As previous years, Saturday afternoon reserved for a...
Abstract Non-small cell lung cancer (NSCLC) is the leading cause of related death, and its major histotypes are adenocarcinoma (ADC) squamous carcinoma (SCC). Nintedanib (Vargatef) a multi-tyrosine kinase inhibitor VEGF, FGF PDGF receptors that has been approved as second-line treatment advanced patients, owing to positive therapeutic effects reported selectively on ADC but not SCC patients in LUME-1 clinical trial. also treat idiopathic pulmonary fibrosis due antifibrotic INPULSIS Of note,...
<div>Abstract<p>The tumor-promoting fibrotic stroma rich in tumor-associated fibroblasts (TAF) is drawing increased therapeutic attention. Intriguingly, a trial with the antifibrotic drug nintedanib non–small cell lung cancer reported clinical benefits adenocarcinoma (ADC) but not squamous carcinoma (SCC), even though both histotypes. Likewise, we that inhibited phenotype of TAFs selectively ADC. Here show tumor fibrosis actually higher ADC-TAFs than SCC-TAFs <i>in...
<p>Supplementary Material</p>
<p>Supplementary Figures S1-S7</p>
<p>Supplementary Figures S1-S7</p>
<p>Supplementary Material</p>
Abstract Adenocarcinoma (ADC) and Squamous Cell Carcinoma (SCC) are the most frequent histologic subtypes of lung cancer, both rich in activated/myofibroblast-like tumor-associated fibroblasts (TAFs). Nintedanib is a potent antifibrotic drug that targets tumor stroma clinically approved to treat advanced ADC patients owing survival benefits observed LUME-1 clinical trial but not SCC patients. Although mechanism underlying ADC-selective therapeutic effects nintedanib remained poorly...
Abstract Background: Lung adenocarcinoma (ADC) and squamous cell carcinoma (SCC) are the most common histologic subtypes in lung cancer. Intriguingly, ADC SCC exhibit distinct responses to multi-tyrosine kinase inhibitor nintedanib other antiangiogenic drugs, suggesting that angiogenesis may depend on subtype In addition, tumor-associated fibroblasts (TAFs) known regulators of angiogenesis, we have recently reported TAFs enhanced fibrosis response compared SCC, owing stronger epigenetic...
<div>Abstract<p>The tumor-promoting fibrotic stroma rich in tumor-associated fibroblasts (TAF) is drawing increased therapeutic attention. Intriguingly, a trial with the antifibrotic drug nintedanib non–small cell lung cancer reported clinical benefits adenocarcinoma (ADC) but not squamous carcinoma (SCC), even though both histotypes. Likewise, we that inhibited phenotype of TAFs selectively ADC. Here show tumor fibrosis actually higher ADC-TAFs than SCC-TAFs <i>in...
Abstract A hallmark of non-small cell lung cancer (NSCLC) is a fibrotic/desmoplastic stroma rich in activated fibroblasts, which are critical regulators progression, response to therapies and radiotherapy resistance. Paradoxically, we recently reported that the important pro-fibrotic TGF-β transcription factor SMAD3 was epigenetically down-regulated through promoter hypermethylation tumor associated fibroblasts (TAFs) from NSCLC patients compared patient-matched control fibroblasts. In...
A hallmark of non-small cell lung cancer (NSCLC) is a fibrotic/desmoplastic stroma rich in activated fibroblasts, which are critical regulators progression, response to therapies and radiotherapy resistance. Paradoxically, we recently reported that the important pro-fibrotic TGF-β transcription factor SMAD3 was epigenetically down-regulated through promoter hypermethylation tumor associated fibroblasts (TAFs) from NSCLC patients compared patient-matched control fibroblasts. In addition,...