Annuaire scientifique



Chargé de Mission CSM et Responsable de l'Équipe Hypoxie Tumorale et Métabolisme
Tel. +377 97 77 44 06
Email : [javascript protected email address]
CV 2018

Thèmes de recherche développés

- Signalisation hypoxique et Stress nutritionnel des cancers
- Les symporters H+/Lactate et le transporteur d’acides aminés (LAT1)
- Validation de nouvelles cibles anticancer

Over the years, Pouyssegur’s group has combined genetics and molecular biology to study the mechanisms of action of growth factors and has characterized the major signaling pathways controlling cell proliferation. His team has made a substantial contribution to the areas of cell surface glycoproteins, metabolism, intracellular pH regulation, identification of human Na/H exchangers and establish that intracellular pH and MAP kinase (ERKs) signaling are critical for cell cycle entry.
During the last 15 years the group has turned its interest to another essential growth mechanism: how do cells control their nutrient supply? This key process has led him to investigate mechanisms of hypoxia signaling, angiogenesis, nutritional stress and aberrant metabolism in tumours.
Currently Pouyssegur’s group pursues, at a fundamental level, the physiological role for key targets induced by nutritional stress and hypoxia in tumors. The focus is on tumor aberrant glucose metabolism (Warburg effect), glycolysis, autophagy, nutrient import driven by HIF, with a special interest in translational research. Numerous anticancer targets disrupted by ZFN & CRISPR/Cas9 are in the process of being validated in preclinical mouse models, by this team (carbonic anhydrases CA9, CA12, CA2, bicarbonate transporters NBCs, MonoCarboxylate Transporters MCT1, MCT4, their chaperone CD147/Basigin and amino acid transporters LAT1/CD98, xCT, ASCT2…). These targets all share a common participation to the ‘Darwinian’ tumour selection and progression within the hypoxic, acidic and nutrient deprived tumour microenvironment.
Metrics : Web of Science citations : 42000, h-factor : 117, Google Scholar : h-factor 126