CircRAD18 promotes glioblastoma proliferation, migration and invasion via the miR‑1231/LUC7L2 axis

Glioblastoma (GBM) is an exceptionally aggressive and malignant central nervous system tumor with a poor prognosis. Studies suggest that circular RNAs (circRNAs) play a vital role in GBM progression. Exosomes, key mediators of intercellular communication, carry circRNAs that may regulate this process. The present study aimed to investigate how circRAD18 modulates GBM cell proliferation, migration and invasion through the miR‑1231/LUC7L2 axis and to evaluate the potential of exosomal circRAD18 as a diagnostic biomarker for GBM. Bioinformatics analyses identified differentially expressed circRAD18, miR‑1231 and LUC7L2 in GBM and predicted their interactions. Expression levels were assessed using western blot analysis, immunohistochemistry and reverse transcription‑quantitative polymerase chain reaction. Regulatory mechanisms were examined via dual‑luciferase reporter assays, RNA pull‑down assays, CCK‑8 assays, wound healing assays, Transwell assays, fluorescence in situ hybridization and subcutaneous xenograft tumor models in nude mice. Exosomes were isolated by ultracentrifugation and characterized using transmission electron microscopy and nanoparticle tracking analysis. circRAD18 expression was markedly upregulated in GBM samples and cell lines. Knockdown of circRAD18 markedly inhibited GBM cell proliferation, migration and invasion both in vitro and in vivo. Suppression of miR‑1231 or overexpression of LUC7L2 enhanced GBM cell proliferation, migration and invasion in vitro, but these effects were counteracted by simultaneous circRAD18 knockdown. Additionally, exosomes derived from GBM cells contained high levels of circRAD18. circRAD18 promotes GBM proliferation, migration and invasion by regulating the miR‑1231/LUC7L2 axis. Given its substantial expression in GBM‑derived exosomes, circRAD18 holds promise as both a therapeutic target and a diagnostic biomarker for GBM.