{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["25(10)"],"submitter":["Andre-Gregoire G"],"pubmed_abstract":["Extracellular vesicles (EVs) are lipid-based nanosized particles that convey biological material from donor to recipient cells. EVs play key roles in glioblastoma progression because glioblastoma stem-like cells (GSCs) release pro-oncogenic, pro-angiogenic, and pro-inflammatory EVs. However, the molecular basis of EV release remains poorly understood. Here, we report the identification of the pseudokinase MLKL, a crucial effector of cell death by necroptosis, as a regulator of the constitutive secretion of EVs in GSCs. We find that genetic, protein, and pharmacological targeting of MLKL alters intracellular trafficking and EV release, and reduces GSC expansion. Nevertheless, this function ascribed to MLKL appears independent of its role during necroptosis. <i>In vivo</i>, pharmacological i"],"journal":["iScience"],"pagination":["105118"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9519628"],"repository":["biostudies-literature"],"pubmed_title":["Inhibition of the pseudokinase MLKL alters extracellular vesicle release and reduces tumor growth in glioblastoma."],"pmcid":["PMC9519628"],"pubmed_authors":["Dupont A","Goetz JG","Rosinska S","Jacobs KA","Thys A","Hyenne V","Andre-Gregoire G","Spinelli F","Bidere N","Cavalli FMG","Trillet K","Maghe C","Douanne T","Busnelli I","Gavard J","Lyne AM","Ballu C"],"additional_accession":[]},"is_claimable":false,"name":"Inhibition of the pseudokinase MLKL alters extracellular vesicle release and reduces tumor growth in glioblastoma.","description":"Extracellular vesicles (EVs) are lipid-based nanosized particles that convey biological material from donor to recipient cells. EVs play key roles in glioblastoma progression because glioblastoma stem-like cells (GSCs) release pro-oncogenic, pro-angiogenic, and pro-inflammatory EVs. However, the molecular basis of EV release remains poorly understood. Here, we report the identification of the pseudokinase MLKL, a crucial effector of cell death by necroptosis, as a regulator of the constitutive secretion of EVs in GSCs. We find that genetic, protein, and pharmacological targeting of MLKL alters intracellular trafficking and EV release, and reduces GSC expansion. Nevertheless, this function ascribed to MLKL appears independent of its role during necroptosis. <i>In vivo</i>, pharmacological i","dates":{"release":"2022-01-01T00:00:00Z","publication":"2022 Oct","modification":"2025-05-18T12:48:48.453Z","creation":"2025-05-18T12:48:48.453Z"},"accession":"S-EPMC9519628","cross_references":{"pubmed":["36185361"],"doi":["10.1016/j.isci.2022.105118"]}}