Radioresistance is a clinical barrier to endometrial cancer (EC) therapy and causes tumor recurrence. In this investigation, researchers discovered that tumor-associated macrophages (TAMs) enriched in EC specimens were determined to present an M2-like phenotype. In vitro, coculture of M2-polarized macrophages dramatically reduced EC cell radiosensitivity by releasing exosomes. Hsa_circ_0001610 was discovered to be abundant in exosomes generated from M2-polarized macrophages (EXOs), and hsa_circ_0001610 knockdown abolished the lowering impact of EXOs on EC cell radiosensitivity. The mechanism investigation demonstrated that hsa_circ_0001610 functioned as the competitive endogenous RNA of miR-139-5p, upregulating cyclin B1 production, which is a critical driver of radioresistance in numerous forms of cancer via regulating the cell cycle. Overexpression of hsa_circ_0001610 decreased radiosensitivity in EC cells, which was later reversed by overexpression of miR-139-5p. TAM-derived exosomes carried hsa_circ_0001610 to EC cells, and the overexpressed hsa_circ_0001610 in EC cells unleashed cyclin B1 expression by adsorbing miR-139-5p, reducing EC radiosensitivity.