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… Click to show full abstract
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 β-catenin and suppressed the transcriptional activity of Wnt/β-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 downregulation of FGF19/Wnt/β-catenin signaling, highlighting an importance of miR-520e/FGF19/Wnt/β-catenin signaling in gliomagenesis and suggesting miR-520e as a potential therapeutic target for gliomas.
               
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