A5059376263- Cancer, Hypoxia, and Metabolism
- Nitric Oxide and Endothelin Effects
- Caveolin-1 and cellular processes
- Angiogenesis and VEGF in Cancer
- Mitochondrial Function and Pathology
- Amino Acid Enzymes and Metabolism
- Cancer, Lipids, and Metabolism
- Ion Transport and Channel Regulation
- Advanced MRI Techniques and Applications
- ATP Synthase and ATPases Research
- Metabolism, Diabetes, and Cancer
- Nanoparticle-Based Drug Delivery
- Nanoplatforms for cancer theranostics
- Diet and metabolism studies
- MRI in cancer diagnosis
- Ion channel regulation and function
- Adipose Tissue and Metabolism
- Metabolomics and Mass Spectrometry Studies
- Electron Spin Resonance Studies
- Immune cells in cancer
- Peroxisome Proliferator-Activated Receptors
- Radiopharmaceutical Chemistry and Applications
- Inflammatory mediators and NSAID effects
- Synthesis and biological activity
- Medical Imaging Techniques and Applications
Walloon Excellence in Lifesciences and Biotechnology
2022-2025
UCLouvain
2015-2024
Directorate-General Joint Research Centre
2016-2024
Cornell University
2019
University of Surrey
2018
Royal Surrey County Hospital
2018
Association Pharmaceutique Belge
2018
Aixtron (Germany)
2010-2017
KU Leuven
2002-2015
Leiden University Medical Center
2012
Tumors contain oxygenated and hypoxic regions, so the tumor cell population is heterogeneous. Hypoxic cells primarily use glucose for glycolytic energy production release lactic acid, creating a lactate gradient that mirrors oxygen in tumor. By contrast, have been thought to oxidative production. Although generally considered waste product, we now show it prominent substrate fuels metabolism of cells. There therefore symbiosis which mutually regulate their access metabolites. We identified...
Lactate generated from pyruvate fuels production of intracellular NAD(+) as an end result the glycolytic process in tumors. Elevated lactate concentration represents a good indicator metabolic adaptation tumors and is actually correlated to clinical outcome variety human cancers. In this study, we investigated whether could directly modulate endothelial phenotype thereby tumor vascular morphogenesis perfusion. We found that enter cells through monocarboxylate transporter MCT-1, trigger...
The endothelial isoform of nitric oxide synthase (eNOS) modulates cardiac myocyte function and is expressed in the particulate subcellular fraction. We have previously shown that eNOS targeted to plasmalemmal caveolae cells. Caveolae, specialized domains plasma membrane, may serve sequester signaling proteins; a family transmembrane proteins, caveolins, form key structural component these microdomains. Caveolae tissues contain muscle-specific caveolin-3, cells widely caveolin-1, which shares...
The endothelial nitric-oxide synthase (eNOS) is a key determinant of vascular homeostasis. Like all known synthases, eNOS enzyme activity dependent on Ca<sup>2+</sup>-calmodulin. dynamically targeted to specialized cell surface signal-transducing domains termed plasmalemmal caveolae and interacts with caveolin, an integral membrane protein that comprises structural component caveolae. We have previously reported the association between caveolin quantitative tissue-specific (Feron, O.,...
Metastatic progression of cancer is associated with poor outcome, and here we examine metabolic changes underlying this process. Although aerobic glycolysis known to promote metastasis, have now identified a different switch primarily affecting mitochondria. The involves overload the electron transport chain (ETC) preserved mitochondrial functions but increased superoxide production. It provides metastatic advantage phenocopied by partial ETC inhibition, another situation enhanced Both cases...
Switching to a glycolytic metabolism is rapid adaptation of tumor cells hypoxia. Although this metabolic conversion may primarily represent rescue pathway meet the bioenergetic and biosynthetic demands proliferating cells, it also creates gradient lactate that mirrors oxygen in tumors. More than waste, anion known participate cancer aggressiveness, part through activation hypoxia-inducible factor-1 (HIF-1) cells. Whether directly favor HIF-1 endothelial (ECs) thereby offering new druggable...
Background —Hypercholesterolemia is causally associated with defects of endothelial nitric oxide (NO)–dependent vasodilation. Increased uptake cholesterol by cells (ECs) upregulates the abundance structural protein caveolin-1 and impairs NO release through stabilization inhibitory heterocomplex between synthase (eNOS). Therefore, we examined whether hydroxy-methylglutaryl–coenzyme A reductase inhibitor atorvastatin modulates caveolin abundance, eNOS activity, a reduction in endogenous...
Hypercholesterolemia is a central pathogenic factor of endothelial dysfunction caused in part by an impairment nitric oxide (NO) production through mechanisms that remain poorly characterized. The activity the isoform NO synthase (eNOS) was recently shown to be modulated its reciprocal interactions with stimulatory Ca2+–calmodulin complex and inhibitory protein caveolin. We examined whether hypercholesterolemia may reduce alteration this regulatory equilibrium. Bovine aortic cells were...
Metabolites released by the gut microbiota may influence host metabolism and immunity. We have tested hypothesis that inulin-type fructans (ITF), promoting microbial production of short-chain fatty acids (SCFA), cancer cell proliferation outside gut. Mice transplanted with Bcr-Abl-transfected BaF3 cells, received ITF in their drinking water. Gut was analysed 16S rDNA polymerase chain reaction (PCR)–denaturing gradient gel electrophoresis (DGGE) qPCR. Serum Short-chain were quantified...
Acidosis, a common characteristic of the tumor microenvironment, is associated with alterations in metabolic preferences cancer cells and progression disease. Here we identify TGF-β2 isoform at interface between these observations. We document that acidic pH promotes autocrine signaling, which turn favors formation lipid droplets (LD) represent energy stores readily available to support anoikis resistance cell invasiveness. find that, various origins, acidosis-induced activation both partial...
Cancer can be envisioned as a metabolic disease driven by pressure selection and intercellular cooperativeness. Together with anaerobic glycolysis, the Warburg effect, formally corresponding to uncoupling glycolysis from oxidative phosphorylation, directly participates in cancer aggressiveness, supporting both tumor progression dissemination. The transcription factor hypoxia-inducible factor-1 (HIF-1) is key contributor glycolysis. It stimulates expression of glycolytic transporters enzymes...