Abstract
Increasing evidence reveals that circular RNAs (circRNAs) regulate multiple biological functions in glioma. Previously, several reports have illustrated that circFAM53B contributes to cancer development. However, the functions and mechanisms of circFAM53B in glioma remain elusive. Here, we gauged the circFAM53B profile in glioma tissues and cell lines and conducted gain-of-function assays of circFAM53B to verify circFAM53B's influence on the proliferation and metastasis of glioma cells (including A172 and LN18). As a result, circFAM53B was up-regulated in glioma tissues (vs. the matched non-tumor tissues). Higher levels of circFAM53B predicted poorer survival of glioma patients. Functionally, circFAM53B up-regulation accelerated cell proliferation, colony formation, invasion and epithelial-mesenchymal transition (EMT), and heightened Bax/Bcl2 ratio. By contrast, circFAM53B down-regulation repressed glioma development in vitro. Mechanistically, bioinformatics analysis suggested that circFAM53B served as a competitive endogenous RNA (ceRNA) by sponging miR-532-3p, which targeted proto-oncogene (MET) and receptor tyrosine kinase (c-MET). miR-532-3p up-regulation delayed glioma development and inactivated the PI3K/AKT axis. Moreover, the treatment of the c-MET inhibitor SGX523, the PI3K inhibitor LY294002, and the Akt inhibitor MK-2206 reduced circFAM53B-mediated oncogenic effects. Conclusively, circFAM53B aggravated glioma progression by up-regulating the c-MET/PI3K/AKT pathway and down-regulating miR-532-3p. Thus, the circFAM53B/miR-532-3p/c-MET/PI3K/AKT axis is a potential treatment target for glioma.