<p>Uveal melanoma (UVM) is the most common primary intraocular human malignancy with a poor prognosis and high mortality rate. Long non-coding RNAs (lncRNAs) and microRNAs (miRNAs) regulate UVM progression through competing endogenous RNA (ceRNA) networks. Ferroptosis is a new form of cell death and a key mechanism involved in the anti-cancer effects of traditional therapies. Although MAPRE2 is known to be an important oncogene in UVM, whether it regulates UVM development via ferroptosis-related ceRNA mechanisms remains unclear. Bioinformatics analyses were used to construct the ceRNA network related to ferroptosis in UVM. Dual-luciferase reporter assay, CCK-8 assay, cell apoptosis assay and other experiments were performed to substantiate our findings. We identified that the AC079193.2/miR 125b 5p axis drives MAPRE2 expression, thereby promoting malignant progression in UVM. Gene enrichment and phenotypic analyses demonstrated that changes in AC079193.2/miR-125b-5p/MAPRE2 expression regulate UVM cell proliferation and apoptosis of UVM cells. Dual-luciferase reporter gene assay demonstrated that AC079193.2 acts as a ceRNA for miR 125b 5p to regulate MAPRE2 expression. In addition, the regulatory effects of AC079193.2 on UVM malignancy were found to depend, at least partially, on MAPRE2. Finally, the ferroptosis-related prognostic model constructed in this study efficiently predicted the prognosis of UVM. This study reveals a novel ceRNA regulatory network in UVM and proposes potential targets for the diagnosis and treatment of UVM.</p>