Circ_PRDM5/miR‐25‐3p/ANKRD46 axis is associated with cell malignant behaviors in subjects with breast cancer evaluated by ultrasound

Abstract

AbstractCircular RNAs (circRNAs) are key RNA molecules in cancer biology. CircRNA PR/SET domain 5 (circ_PRDM5, hsa_circ_0005654) was downregulated in breast cancer (BC) tissues. This study is designed to investigate the functional mechanism of circ_PRDM5 in BC. Ultrasound examinations were performed to evaluate BC patients and normal individuals. Circ_PRDM5, miR‐25‐3p, and Ankyrin repeat domain 46 (ANKRD46) level detection was carried out by reverse transcription‐quantitative polymerase chain reaction. 3‐(4, 5‐dimethylthiazol‐2‐y1)‐2, 5‐diphenyl tetrazolium bromide (MTT) assay was used for cell viability examination. Cell proliferation was evaluated by ethynyl‐2′‐deoxyuridine assay and colony formation assay. The protein levels were examined using western blot. Cell migration and invasion abilities were assessed via transwell assay. Target interaction was analyzed via dual‐luciferase reporter assay. The role of circ_PRDM5 in vivo was explored via xenograft tumor assay. Circ_PRDM5 expression was downregulated in BC tissues and cells. Overexpression of circ_PRDM5 suppressed proliferation and motility but enhanced apoptosis of BC cells. Circ_PRDM5 served as a sponge of miR‐25‐3p. Circ_PRDM5 impeded BC cell malignant development via sponging miR‐25‐3p. Circ_PRDM5 induced ANKRD46 upregulation by targeting miR‐25‐3p. Inhibition of miR‐25‐3p retarded BC progression by increasing the ANKRD46 level. Circ_PRDM5 repressed BC tumorigenesis in vivo through mediating the miR‐25‐3p/ANKRD46 axis. This study evidenced that circ_PRDM5 inhibited cell progression and tumor growth in BC via interacting with mir‐25‐3p/ANKRD46 network.