ARAP3 Facilitates Glioma Progression via IGF2BP3-Mediated m6A Modification Stabilization

N6-methyladenosine (m6A)-dependent post-transcriptional regulation is increasingly recognized as a key driver of malignant progression. However, the role and regulatory mechanism of ARAP3 in glioma remain incompletely understood. ARAP3 expression was analyzed in 112 paired glioma and adjacent tissues by qRT-PCR and Western blot. Its diagnostic and clinical relevance were evaluated using ROC analysis and clinicopathological correlation. Gain- and loss-of-function assays were performed in U87 and U251 cells to assess proliferation, clonogenicity, and invasion. IGF2BP3-dependent regulation was examined through lentiviral shRNA-mediated knockdown, RNA immunoprecipitation, m6A RNA immunoprecipitation, and actinomycin D mRNA decay assays. Xenograft models were used to validate in vivo effects. ARAP3 was significantly upregulated in glioma tissues and correlated with larger tumor size and higher WHO grade, demonstrating good diagnostic performance (AUC = 0.83). High ARAP3 predicted worse survival in TCGA glioblastoma and LGG cohorts. Silencing ARAP3 suppressed glioma cell growth, colony formation, and invasion. Mechanistically, IGF2BP3 bound to ARAP3 mRNA, maintained its m6A-dependent enrichment, and enhanced transcript stability. Overexpression of ARAP3 partially rescued the inhibitory effects of IGF2BP3 knockdown in vitro and in vivo. In the xenograft model, no obvious metastatic nodules or infiltrative lesions were observed in major organs, including the lungs, liver, spleen, kidneys, and brain. ARAP3 promotes glioma progression and is sustained by IGF2BP3-mediated m6A-dependent mRNA stabilization, highlighting the IGF2BP3-ARAP3 axis as a potential biomarker and therapeutic target.