Background. Gliomas are the most common and most malignant primary tumors of the adult central nervous system, but their etiology and pathogenesis remain unclear. This study was aimed at investigating the expression and function of lncRNA PDCD4-AS1 in glioma and elucidating the mechanism by which PDCD4-AS1 regulates the biological features of glioma. Method. The expression of PDCD4-AS1 was determined by bioinformatic analysis and qRT-PCR assay. PDCD4-AS1 was knocked down in glioma cells using siRNA transfection. The functional analysis of cells was conducted using CCK-8 proliferation, cell migration, and invasion assays, as well as cell cycle analysis. An in vivo tumorigenesis assay was performed to investigate the role of PDCD4-AS1 knockdown in glioma tumor growth. We performed bioinformatic analysis, RNA pull-down, and luciferase reporter assays to investigate the downstream targets of PDCD4-AS1. A rescue experiment was then performed to confirm the regulating mechanism. Results. PDCD4-AS1 was found to be significantly upregulated in glioma patients’ tumor tissues and cell lines. The silencing of PDCD4-AS1 inhibited glioma cell proliferation, invasion, migration, and induced cell cycle arrest. In vivo experiments showed that silencing PDCD4-AS1 inhibited glioma tumor growth. An investigation of the underlying mechanism suggested that PDCD4-AS1 positively regulated METTL7B expression by sponging miR-30b-3. Both the knockdown of miR-30b-3p and the overexpression of METTL7B could, respectively, reverse the malignant phenotype of cells affected by silencing PDCD4-AS1. Conclusion. These results demonstrate that PDCD4-AS1 exerted an oncogenic role by regulating the miR-30b-3p/METTL7B axis.