{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Menga A"],"funding":["European Research Council","Fonds Wetenschappelijk Onderzoek"],"pagination":["e51981"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8419692"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(9)"],"pubmed_abstract":["Glutaminolysis is known to correlate with ovarian cancer aggressiveness and invasion. However, how this affects the tumor microenvironment is elusive. Here, we show that ovarian cancer cells become addicted to extracellular glutamine when silenced for glutamine synthetase (GS), similar to naturally occurring GS-low, glutaminolysis-high ovarian cancer cells. Glutamine addiction elicits a crosstalk mechanism whereby cancer cells release N-acetylaspartate (NAA) which, through the inhibition of the NMDA receptor, and synergistically with IL-10, enforces GS expression in macrophages. In turn, GS-high macrophages acquire M2-like, tumorigenic features. Supporting this in␣vitro model, in silico data and the analysis of ascitic fluid isolated from ovarian cancer patients prove that an M2-like macro"],"journal":["EMBO reports"],"pubmed_title":["N-acetylaspartate release by glutaminolytic ovarian cancer cells sustains protumoral macrophages."],"pmcid":["PMC8419692"],"funding_grant_id":["G0D1717N","G066515N","773208"],"pubmed_authors":["Mazzone M","De Grassi A","Menga A","Canton M","Spera I","Gissi R","Cormio G","Carra G","Favia M","Castegna A","Laera L","Vegliante MC","Campanella A","Gerbino A","Loizzi V","Pierri CL"],"additional_accession":[]},"is_claimable":false,"name":"N-acetylaspartate release by glutaminolytic ovarian cancer cells sustains protumoral macrophages.","description":"Glutaminolysis is known to correlate with ovarian cancer aggressiveness and invasion. However, how this affects the tumor microenvironment is elusive. Here, we show that ovarian cancer cells become addicted to extracellular glutamine when silenced for glutamine synthetase (GS), similar to naturally occurring GS-low, glutaminolysis-high ovarian cancer cells. Glutamine addiction elicits a crosstalk mechanism whereby cancer cells release N-acetylaspartate (NAA) which, through the inhibition of the NMDA receptor, and synergistically with IL-10, enforces GS expression in macrophages. In turn, GS-high macrophages acquire M2-like, tumorigenic features. Supporting this in␣vitro model, in silico data and the analysis of ascitic fluid isolated from ovarian cancer patients prove that an M2-like macro","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 Sep","modification":"2026-05-08T10:14:32.284Z","creation":"2022-02-11T10:59:19.637Z"},"accession":"S-EPMC8419692","cross_references":{"pubmed":["34260142"],"doi":["10.15252/embr.202051981"]}}