Background and Aims Ferroptosis is an iron-dependent form of regulated cell death characterized by lipid peroxidation and has potential applications in colorectal cancer (CRC) therapy. Circular RNAs (circRNAs) can regulate tumor progression through competing endogenous RNA (ceRNA) mechanisms; however, their roles and regulatory mechanisms in CRC ferroptosis remain incompletely understood. This study aimed to identify dysregulated circRNAs in CRC, investigate the effects of hsa_circ_0001819 (circ1819) on ferroptosis and malignant phenotypes of CRC cells, and preliminarily explore its potential molecular mechanism.Methods CircRNA microarray datasets GSE223001 and GSE205643 were integrated to identify differentially expressed circRNAs, with GSE126094 used for validation. The expression of circ1819 in CRC tissues and cell lines was examined by qRT-PCR. RNase R digestion, actinomycin D treatment, and nuclear-cytoplasmic fractionation assays were performed to characterize its circular structure, stability, and subcellular localization. Following siRNA-mediated circ1819 knockdown, cell viability, lipid reactive oxygen species (ROS), malondialdehyde (MDA), and ferroptosis-related proteins were assessed in the presence of the ferroptosis inducer RSL3 and inhibitor Liproxstatin-1 (Lip-1). CCK-8, colony formation, and Transwell assays were used to evaluate cell proliferation and migration. AGO2 RNA immunoprecipitation (AGO2-RIP), RNA pulldown, and bioinformatics analyses were performed to investigate the potential ceRNA regulatory mechanism of circ1819.Results Circ1819 was significantly upregulated in CRC tissues and cell lines, and its expression was associated with tumor diameter and T stage. Circ1819 exhibited typical characteristics of a circular RNA and was predominantly localized in the cytoplasm. Circ1819 knockdown significantly increased the sensitivity of CRC cells to RSL3-induced ferroptosis, as evidenced by reduced cell viability and increased lipid ROS and MDA levels; these effects were partially reversed by Lip-1. Circ1819 knockdown significantly reduced GPX4 mRNA and protein expression, whereas SLC7A11 and ACSL4 expression remained unchanged. Moreover, circ1819 knockdown significantly inhibited CRC cell proliferation, colony formation, and migration. AGO2-RIP and RNA pulldown assays suggested interactions between circ1819 and miR-618 or miR-1231. Combined with target prediction and enrichment analyses, a potential circ1819-centered circRNA-miRNA-mRNA regulatory network was constructed.Conclusion Circ1819 is aberrantly upregulated in CRC, and its knockdown enhances ferroptosis sensitivity while suppressing proliferation and migration of CRC cells. These effects may be associated with ceRNA regulation involving miR-618 and miR-1231 and alterations in GPX4 expression. Circ1819 may represent a potential regulatory link between malignant progression and ferroptosis resistance in CRC, although its downstream targets and causal regulatory relationships require further validation.