The m6A-Mediated LINC00857 Upregulation Facilitates Glioma Migration, Invasion and Vasculogenic Mimicry Formation

Abstract

LINC00857 and m6A methylation were validated to be clearly elevated in glioma patient tumor samples and cell lines. We found that silenced the LINC00857 gene repressed vasculogenic mimicry (VM) formation and VM-linked protein expression in glioma cells, and depressed three processes closely implicated with VM formation—migration, invasion, and epithelial-mesenchymal transition (EMT). Meanwhile, VM was also restrained by silencing of LINC00857. To figure out LINC00857's latent functions in glioma and its molecular mechanism, it was further testified that miR-202-3p was LINC00857's target through biological prediction website, the luciferase activity and RNA immunoprecipitation (RIP) assay. Furthermore, elevation of miR-202-3p caused downregulation of HMGA2, which is recognized as miR-202-3p's downstream target. In conclusion, this study clarified m6A mediated the upregulation of LINC00857, and enhanced VM formation in glioma cells by negatively regulating miR-202-3p and motivating HMGA2. LINC00857 may be a new therapeutic target for VM formation in glioma.