ArticleiScience2022
Inhibition of the pseudokinase MLKL alters extracellular vesicle release and reduces tumor growth in glioblastoma.
Article in iScience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Mechanistic analysis of MLKL-driven cell survival.Cell death discovery · 2026Review
- Stress granules restrain ferroptosis by sequestering ferritin.Nature cell biology · 2026Article
- Lipopolysaccharides Drive Proinflammatory Extracellular Vesicle Secretion in Coronary Artery Endothelial Cells via Noncanonical Inflammasome Activation.Cellular and molecular life sciences : CMLS · 2026Article
- MLKL depletion enhances chemotherapy-induced apoptosis in colorectal cancer by prolonged retention of TNFR-I in endosomes.Apoptosis : an international journal on programmed cell death · 2026Article
- Recent Advances of Small Extracellular Vesicles for the Regulation and Function of Cancer-Associated Fibroblasts.International journal of molecular sciences · 2024Review
- Article
- Dysregulation of intercellular communication in vitro and in vivo via extracellular vesicles secreted by pancreatic duct adenocarcinoma cells and generated under the influence of the AG9 elastin peptide-conditioned microenvironment.Journal of extracellular biology · 2024Article
Corrections and comments
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Authors and funding
17 authors.
Funding
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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.
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Registered trials
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