Increasing research has indicated that circular RNAs (circRNAs) are crucial for the development of ulcerative colitis (UC). Thus, we attempted to identify the role of hsa_circ_0004662 in UC progression. Hsa_circ_0004662 expression was determined via qRT-PCR. Lipopolysaccharide (LPS)-induced inflammation in normal colonic epithelial cells (ECs). The hsa_circ_0004662 content was then assessed in a mucosal inflammatory bowel disease (IBD) model. Cell proliferation was examined via CCK-8 and EdU uptake assays. Apoptotic rates were analysed via flow cytometry. The protein content was quantified via Western blotting. Enzyme-linked immunosorbent assay kits were used to detect IL-1beta, TNF-alpha and IL-6, and dual-luciferase reporter (DLR) assays were used to identify interactions between miR-532 and circ_0004662 or HMGB3. An animal model of UC was also developed for confirmation. In this study, we identified the function of hsa_circ_0004662 in promoting UC progression. Hsa_circ_0004662 was upregulated in clinical UC tissues and LPS-induced colonic ECs, and its knockdown inhibited apoptosis, reduced inflammatory cytokine release and promoted cell proliferation in vitro. Mechanistically, hsa_circ_0004662 acted as a molecular sponge for miR-532, which targets HMGB3. The hsa_circ_0004662/miR-532/HMGB3 axis was further validated in a DSS-induced colitis mouse model, where hsa_circ_0004662 knockdown attenuated inflammation and tissue damage. These findings suggested that hsa_circ_0004662 contributes to UC progression through the miR-532/HMGB3 signalling pathway, offering potential targets for UC therapy.