Circular RNA circSCAF11 accelerates the glioma tumorigenesis through miR-421/SP1/VEGFA axis

Abstract Background Circular RNAs (circRNAs) are a novel category of non-coding RNAs and have been identified to participate in the glioma tumorigenesis. Here, we investigate the functions of circRNA circSCAF11 in the gliomagenesis and unveil its molecular mechanism of the pathophysiological process. Methods Expression levels of circSCAF11, miR-421 and SP1 mRNA were measured using RT-PCR. Proteins were measured using western blotting. The tumor phenotypes of glioma cells were detected using CCK-8, flow cytometry, transwell and xenograft mice assay. The combination within circSCAF11, miR-421 and SP1 was validated using luciferase reporter assay or RNA pull down assay. The binding of transcription factor SP1 with VEGFA promoter was inspected using chromatin immunoprecipitation (ChIP). Results circSCAF11 expression was found to be significantly up-regulated in the glioma tissue specimens and cell lines. The ectopic overexpression of circSCAF11 was closely correlated with the poor clinical outcome of glioma patients. Functionally, knockdown of circSCAF11 inhibited the proliferation, invasion, tumor growth and induced the G0/G1 phase arrest. Mechanically, circSCAF11 positively regulated the SP1 expression through sponging miR-421. Moreover, transcription factor SP1 activated the transcription of VEGFA, constructing circSCAF11 /miR-421/SP1/VEGFA axis in the gliomagenesis. Conclusion The findings in this research illustrate that circSCAF11 accelerates the glioma tumorigenesis through miR-421/SP1/VEGFA axis, providing a potential targets for circRNA and glioma treatment.