Le vendredi 5 juin 2026, Madame Coline WERY, titulaire d'un Master en biochimie, biologie cellulaire et moléculaire et d'un Certificat de formation à la recherche en sciences biomédicales et pharmaceutiques présentera l'examen en vue de l'obtention du grade de Doctorat en sciences biomédicales et pharmaceutiques sous la direction de Monsieur Nor Eddine SOUNNI.

Cette épreuve consistera en la défense publique d'une thèse intitulée : "Exploration des mécanismes impliquant les gouttelettes lipidiques et la stéaroyl-CoA désaturase (SCD) dans la progression du cancer". 

Le jury sera composé de :

Franck DEQUIEDT (Président), Benaïssa EL MOUALIJ (Secrétaire), Pierre CLOSE, Olivier FERON (UCLouvain), Elisabeth LETELLIER (Univ. Luxembourg), Agnès Noël, Nor Eddine SOUNNI, 

Résumé de la thèse

Tumor hypoxia induces metabolic changes in cancer cells and cancer malignancy. We recently reported that induced-tumor hypoxia in vivo enhances fatty acid storage in lipid droplets (LD), whereas reoxygenation increases lipid desaturation in cancer cells and tumor recurrence. Here we found that Stearoyl-CoA Desaturase-1 (SCD1) and the LD marker, PLIN2 (perilipin-2) are upregulated by hypoxia in cancer cells. Depletion of PLIN2 or SCD1 by CRISPR/Cas9 in MDA-MB231 and HT29 cells resulted in a decreased number of LD in cells under hypoxia, reduced cell migration and proliferation in vitro and reduced tumor growth in vivo. PTM analyses of acetylated proteins in SCD1 and PLIN2 depleted cells revealed a pattern of non-histone proteins acetylation/deacetylation. Notably, nucleophosmin (NPM1), a tumor suppressor protein, was strongly deacetylated in SCD1 expressing cells. CoIP analyses confirmed the role of SCD1 as a potential deacetylase-like protein of NPM1. Interestingly, deacetylation of NPM1 decreases its stabilization and increases it nuclear localization whereas its acetylation induces a cytoplasmic localization. Our results indicate that PLIN2 is involved in increased acetylation of non-histone proteins as a cellular response to hypoxic stress, whereas SCD1 expression led to the deacetylation of tumor suppressor NPM1 and proteins involved in cell migration and cancer progression.