Background: Breast cancer (BC) is a common tumor in women worldwide, and irradiation (IR) resistance is a major obstacle for BC therapy. Circle RNAs (circRNAs) were identified as implicated in the progression of cancer and IR resistance. However, the role of circABCB10 in BC progression and IR resistance is not well defined. Materials and Methods: The levels of circABCB10, miR-223-3p, and profilin-2 (PFN2) were detected by quantitative real-time polymerase chain reaction. The cell viability and survival rate were monitored by MTT assay. The glucose consumption, lactic acid production, LDH-A activity, and ATP production were evaluated to measure glycolysis. The protein levels of hypoxia inducible factor-1α (HIF-1α), hexokinase 2 (HK2), lactate dehydrogenase A chain (LDH-A), and PFN2 were estimated by Western blot assay. The colony formation rate was tested by colony formation assay. Dual-luciferase reporter assay was constructed to validate the interaction between miR-223-3p and circABCB10 or PFN2. The mice xenograft assay was performed to further verify the effects of circABCB10 on BC progression in vivo. Results: CircABCB10 and PFN2 were elevated, while miR-223-3p was reduced in BC tissues and cells. CircABCB10 sponged miR-223-3p, and PFN2 was a target of miR-223-3p in BC cells. CircABCB10 silencing inhibited cell proliferation, glycolysis, colony formation, and decreased IR resistance in BC cells by modulating miR-223-3p. Meanwhile, circABCB10 depletion restrained xenograft tumor growth in vivo. Also, miR-223-3p overexpression refrained cell proliferation, glycolysis, and colony formation while improving IR sensitivity in BC cells by regulating PFN2. Besides, circABCB10 knockdown declined PFN2 in BC cells via miR-223-3p. The glycolysis inhibitor 2-deoxy-D-glucose enhanced IR sensitivity in BC cells via circABCB10. Conclusion: CircABCB10 knockdown contributed to irradiation sensitivity by negatively regulating glycolysis via the miR-223-3p/PFN axis in breast cancer.

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