miR-216b suppresses glioma progression by targeting SREBP1-mediated lipid metabolic reprogramming

Lipid metabolic reprogramming contributes to glioma progression. Although miR-216b has tumor-suppressive effects in glioma, its role in lipid metabolism remains unclear. Gain- and loss-of-function assays assessed its effects on proliferation, colony formation, migration and invasion. Biotin-labelled miRNA pull-down, dual-luciferase reporter and AGO-RIP assays validated the interaction between miR-216b and SREBP1. Triglyceride measurement, BODIPY staining, Oil Red O staining and SREBP1 rescue experiments were performed to evaluate lipid accumulation and functional relevance. miR-216b was markedly downregulated in glioma cell, and its overexpression suppressed malignant phenotypes and lipid accumulation. Mechanistically, miR-216b directly targeted SREBP1 and reduced its expression, while SREBP1 restoration partially rescued lipid accumulation and malignant phenotypes suppressed by miR-216b. miR-216b suppresses glioma progression by targeting SREBP1-mediated lipid metabolic reprogramming, highlighting the miR-216b/SREBP1 axis as a potential therapeutic target in glioma.