RESUMEN
Researches indicate that circular RNAs are dysregulated in breast cancer (BC) and play a critical role in regulating the malignant phenotype of cancer cells. Herein, the goal of this work was to investigate the role and mechanism of circ_0069718 in BC development. Levels of genes and proteins were detected by quantitative real-time polymerase chain reaction and western blot. In vitro experiments were performed using cell counting kit-8 assay, colony formation assay, EdU (5-ethynyl-2'-deoxyuridine) assay, flow cytometry, western blot, and transwell assay, respectively. The dual-luciferase reporter and RNA immunoprecipitation assays were used to identify the target relationship between miR-590-5p and circ_0069718 or nuclear factor I/B (NFIB). In vivo experiments were conducted using Xenograft model in mice. Circ_0069718 was up-regulated in BC tissues and cells. Knockdown of circ_0069718 suppressed BC cell apoptosis, migration, and invasion in vitro effectively. Mechanistically, circ_0069718 directly targeted miR-590-5p to up-regulate its target NFIB. Rescue experiments showed that miR-590-5p inhibition reversed the inhibitory effects of circ_0069718 knockdown on BC cell-aggressive oncogenic phenotypes; moreover, miR-590-5p re-expression restrained BC cell proliferation and mobility, which were abolished by NFIB up-regulation. Besides that, circ_0069718 silencing hindered tumor growth via miR-590-5p/NFIB axis in vivo. Circ_0069718 promotes BC progression by up-regulating NFIB through sequestering miR-590-5p, suggesting a potential therapeutic strategy in BC.