Hsa_circ_0005273 acts as a sponge of miR‐509‐3p to promote the malignant behaviors of breast cancer by regulating HMMR expression

Abstract

AbstractBackgroundBreast cancer (BC) is a common malignant tumor that threatens the health of women worldwide. Hsa_circ_0005273 has been identified as a carcinogenic factor in some solid tumors, including BC. However, the molecular mechanism of circ_0005273 in BC is poorly defined.MethodsThe expression of circ_0005273, miR‐509‐3p, and hyaluronan‐mediated motility receptor (HMMR) mRNA in BC was detected by quantitative real‐time polymerase chain reaction. Cell proliferation, migration, invasion, and apoptosis were detected by 5‐ethynyl‐2′‐deoxyuridine, transwell, and flow cytometry assays. The glycolysis level was detected via specific kits. Western blot was used to detect protein expression. Binding between miR‐509‐3p and circ_0005273 or HMMR was also verified by dual‐luciferase reporter, RNA pull‐down, and RNA immunoprecipitation assays. Xenograft tumor model was used to detect tumor changes in mice, and immunohistochemistry assay was employed to detect Ki‐67 abundance.ResultsCirc_0005273 was increased in BC tissues and cells. Circ_0005273 knockdown might inhibit BC cell proliferation, migration, invasion, glutamine metabolism, and induce apoptosis. Circ_0005273 was a miR‐509‐3p, and the repression role of circ_0005273 absence on BC cell development was weakened by miR‐509‐3p inhibitor or HMMR overexpression. Circ_0005273 up‐regulated the expression of HMMR by sponging miR‐509‐3p. Additionally, circ_0005273 silencing might hinder tumor growth in vivo.ConclusionCirc_0005273 knockdown might repress BC cell malignant behaviors by regulating the miR‐509‐3p/HMMR axis, which might provide a potential therapeutic target for BC.