CircRNAs are critically involved in the progression of numerous cancers, including hepatocellular carcinoma (HCC). While circCOPA has been reported to function as a tumor suppressor in glioblastoma, its role and underlying mechanisms in HCC remain largely unexplored. By analyzing the Gene Expression Omnibus (GEO), we identified a new oncogenic circRNA, hsa_circ_0008661 (circCOPA), which was significantly upregulated in HCC tissues. In a cohort of 80 HCC patients, circCOPA upregulation was associated with poor prognosis and worse clinicopathological characteristics. Functional assays revealed that circCOPA depletion suppressed HCC proliferation and metastasis, whereas circCOPA overexpression exerted opposite effects. RNA sequencing analysis confirmed that circCOPA activated the ERK/MAPK signaling pathway through the downregulation of SPRED2. Mechanistically, RNA pulldown and mass spectrometry analysis demonstrated that circCOPA directly interacted with HNRNPD. This interaction promoted SPRED2 mRNA degradation through binding of HNRNPD to the UGUUU motif within its 3'UTR, leading to SPRED2 downregulation and subsequent activation of the ERK/MAPK signaling pathway. Notably, the oncogenic phenotypes driven by circCOPA were effectively rescued by SPRED2 overexpression. Collectively, our findings delineate a novel circCOPA/HNRNPD/SPRED2 axis that activates the ERK/MAPK signaling pathway to drive HCC progression, highlighting its promise as a novel therapeutic target.