circEFR3A promotes breast cancer progression by sponging miR-590-3p to upregulate androgen receptor expression.

Circular (circ)RNA, a type of non-coding RNA, serves a critical role in several diseases, including cancer. The present study aimed to elucidate the involvement of hsa_circ_0006522 (circEFR3A) in the advancement of breast cancer (BC) and uncover the molecular mechanisms behind its function. Fluorescence in situ hybridization (FISH) was performed on a tissue microarray to assess the expression and intracellular localization of circEFR3A. Kaplan-Meier analysis and Cox proportional hazards model were utilized to evaluate the potential prognostic significance of circEFR3A in relation to the overall survival of patients with BC. The biological function was assessed through gain- and loss-of-function experiments. In addition, dual luciferase reporter assays, RNA immunoprecipitation, FISH and western blotting were performed to identify the interaction between circEFR3A, microRNA (miR)-590-3p and androgen receptors (ARs). Rescue experiments were performed to identify the hypothetical regulatory role of circEFR3A on BC progression in vivo and in vitro. The results of the present study demonstrated that circEFR3A was significantly upregulated in BC tissues and was associated with a poor prognosis in patients. Findings from the Cell Counting Kit-8, colony formation and Transwell assays revealed that increased circEFR3A expression notably promoted BC cell proliferation, invasion and migration, as well as tumor growth in vivo. Mechanistically, circEFR3A was demonstrated to act as a molecular sponge for miR-590-3p in vitro and in vivo, thereby regulating AR expression and functioning as an oncogene. In summary, the findings of the present study indicate that circEFR3A acts as a novel oncogene in BC by sponging miR-590-3p, leading to the upregulation of AR expression and consequently driving BC progression.