The abnormal expression of microRNAs (miRNAs) contributes to the development and progression of cancer. Recent studies have reported that miRNA-520e (miR-520e) is dysregulated in multiple cancers and is associated with tumor progression. However, the role of miR-520e in glioma has not been fully investigated. In this study, we investigated the function of miR-520e and its regulation by a molecular mechanism in gliomas. Our results showed that miR-520e expression was significantly downregulated in glioma tissues and cell lines. The overexpression of miR-520e repressed the proliferation, colony formation, and invasive potential of glioma cells, while the inhibition of miR-520e showed the opposite effect. The oncogenic gene fibroblast growth factor 19 (FGF19) was identified as a downstream target gene of miR-520e. The knockdown of FGF19 restricted the proliferation and invasion of glioma cells. Moreover, FGF19 knockdown or miR-520e overexpression decreased the expression of beta-catenin and suppressed the transcriptional activity of Wnt/beta-catenin signaling. Notably, the restoration of FGF19 expression partially reversed the miR-520e-mediated antitumor effect. In conclusion, our results demonstrate that miR-520e restricts the proliferation and invasion of glioma cells through the down regulation of FGF19/Wnt/beta-catenin signaling, highlighting an importance of miR-520e/FGF19/Wnt/beta-catenin signaling in gliomagenesis and suggesting miR-520e as a potential therapeutic target for gliomas. (C) 2019 Elsevier Inc. All rights reserved.