CircCEP85 upregulates IGF1 expression to promote breast cancer progression via sponging miR-1193

Abstract

Abstract Background Increasing evidence has suggested that circular RNAs (circRNAs) play critical roles in breast cancer (BC) progression. However, the expression level and potential functional role of circRNA centrosomal protein 85 (circCEP85) in BC remains largely unknown. Here, we aimed to explore the role of circCEP85 in BC. Methods The levels of circCEP85, insuline-like growth factor I (IGF1) mRNA and microRNA-1193 (miR-1193) were examined by quantitative real-time polymerase chain reaction. The protein level was measured by Western blot. Cell proliferation, migration, apoptosis, angiogenesis and stemness were assessed by cell counting kit-8, 5-ethynyl-2’-deoxyuridine assay, transwell assay, flow cytometry, tube formation and sphere formation assays. Xenograft mouse models were conducted to evaluate the effect of circCEP85 in BC in vivo. Moreover, dual-luciferase reporter, RNA pull-down, and RNA immunoprecipitation (RIP) assays were preformed to confirm the interaction between miR-1193 and circCEP85 or IGF1. Results CircCEP85 was upregulated in BC tissues and cells. Silencing of circCEP85 inhibited proliferation, invasion, angiogenesis and stemness, but promoted apoptosis in BC cells in vitro. In addition, circCEP85 silencing inhibited tumor growth in vivo. Mechanistically, circCEP85 elevated IGF1 expression via sponging miR-1193 to promote breast cancer progression. Conclusion The circCEP85-miR-1193-IGF1 axis regulated BC progression via the competitive endogenous RNA (ceRNA) mechanism. CircCEP85 might be a prognostic biomarker and therapeutic target for BC.