Background: Hepatocellular carcinoma (HCC) is a type of primary liver cancer with high mortality. Circular RNAs (circRNAs) have been confirmed to be involved in the development of HCC, but the functions of circ_0011232 in HCC remain ill‐defined. Methods: Quantitative real‐time polymerase chain reaction, western blot assay, or immunohistochemistry assay was performed to determine the levels of circ_0011232, miR‐503‐5p, and AKT3. RNase R assay and actinomycin D assay were conducted to analyze the feature of circ_0011232. Cell Counting Kit‐8 assay, 5‐ethynyl‐2′‐deoxyuridine assay, colony formation assay, flow cytometry analysis, wound‐healing assay, and transwell assay were conducted to evaluate HCC cell proliferation, colony formation, apoptosis, migration, and invasion. Dual‐luciferase reporter assay was carried out to confirm the relationships among circ_0011232, miR‐503‐5p, and AKT3. The murine xenograft assay was conducted to verify the function of circ_0011232 in tumor growth in vivo. Results: Circ_0011232 and AKT3 were upregulated, while miR‐503‐5p was decreased in HCC tissues and cells. Circ_0011232 knockdown repressed HCC cell proliferation, colony formation, migration, and invasion, and promoted apoptosis in vitro and blocked tumor growth in vivo. MiR‐503‐5p was a target of circ_0011232. MiR‐503‐5p inhibition reversed the effects of circ_0011232 knockdown on HCC cell development. Moreover, AKT3 was confirmed to be a target of miR‐503‐5p, and AKT3 overexpression abolished the inhibitory effects on HCC cell progression caused by miR‐503‐5p. Conclusion: Circ_0011232 facilitated HCC progression via miR‐503‐5p/AKT3 axis, which might provide a novel treatment strategy for HCC. [ABSTRACT FROM AUTHOR]