Blocking LINC00152 suppresses glioblastoma malignancy by impairing mesenchymal phenotype through the miR-612/AKT2/NF-B pathway

IntroductionGlioblastoma, the most common and mortal primary brain tumor, accompanied with a dismal clinical outcome in adults. The oncogenic functions of long non-coding RNAs (lncRNAs) in glioblastoma have not been completely illuminated. In the present study, we aimed to investigate the potential role of lncRNA LINC00152 in glioblastoma.MethodsWe used bioinformatic method in public databases to select lncRNA LINC00152 and investigate its clinical value and potential mechanism in glioblastoma. CCK-8, transwell assay, colony formation and wound healing assays were used to explore the role of LINC00152 in glioblastoma malignant behaviors. PCR, western blot, immunofluorescence, reporter assays and nude mouse tumor intracranial model were employed to further verify the regulatory mechanism of LINC00152 in glioblastoma.ResultsLINC00152 was closely associated with glioma WHO classification and poor prognosis, and indicated a poor prognosis in glioblastoma patients. Tumor growth and invasion were suppressed both in vitro and vivo after LINC00152 was blocked. Moreover, LINC00152 modulated GBM malignant progression and proneural-mesenchymal transition through the miR-612 dependent AKT2/NF-B pathway.ConclusionsLINC00152 acted as a tumor oncogene with prognostic value for patients with glioblastoma through LINC00152/miR-612/AKT2/NF-B axis.