CircPOSTN competes with KIF1B for miR-185–5p binding sites to promote the tumorigenesis of glioma

Abstract

BackgroundThe involvement of certain circular RNAs (circRNAs) in the development of glioma has been revealed. CircRNA periostin (circPOSTN) was validated to be positively associated with glioma cell growth and metastasis. However, the mechanism underlying circPOSTN in glioma tumorigenesis remain vague. MethodsThe expression of circPOSTN, KIF1B (Kinesin Family Member 1B) and miR-185–5p was detected using quantitative real-time polymerase chain reaction and Western blot. In vitro assays were conducted using cell counting kit-8 assay, colony formation assay, EdU assay, flow cytometry, Western blot, and transwell assay, respectively. The direct interactions between miR-185–5p and circPOSTN or KIF1B was confirmed by using dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. ResultsCircPOSTN was highly expressed in glioma tissues and cells. Knockdown of circPOSTN restrained glioma cell proliferation, migration and invasion in vitro, as well as hindered glioma xenograft growth in vivo. Mechanistically, circPOSTN acted as miR-185–5p sponge to up-regulate the expression of its target KIF1B. Moreover, miR-185–5p inhibition reversed the anticancer effects of circPOSTN knockdown on glioma tumorigenesis, and miR-185–5p re-expression suppressed the malignant phenotype of glioma cells via targeting KIF1B. ConclusionCircPOSTN acted as an oncogene to expedite glioma tumorigenesis via targeting miR-185–5p/KIF1B axis, indicating a potential therapeutic target for glioma.