4-Methylumbelliferone induces oxidative stress-driven metabolic vulnerability and disrupts glycosylation in glioblastoma cells
This study demonstrates that 4-Methylumbelliferone (4MU) exerts antitumor effects in glioblastoma cells by inducing early oxidative stress that depletes NAD⁺, disrupts N-glycosylation, and triggers compensatory metabolic rewiring, thereby revealing a novel mechanism for targeting metabolic vulnerabilities in this aggressive brain tumor.