Hepatoblastoma is the most common liver malignancy in children. Approximately 20% of patients present metastasis at diagnosis and have a dismal prognosis. However, the molecular mechanisms and targeted therapeutic strategies remain limited. Integrated analysis of GSE151347, GSE133039, GSE131329 and GSE75271 datasets, incorporating the mRNA expression-based stemness index, weighted gene co-expression network analysis, ChEA3 and TRRUST databases, receiver operating characteristic (ROC) curve and differential expression analysis, identified forkhead box protein M1 (FOXM1) as a key transcription factor significantly correlated with metastatic hepatoblastoma and poor clinical outcomes. In HuH6 and HepG2 cells, FOXM1 promoted stem cell-like phenotype, migration, invasion and epithelial–mesenchymal transition. In vivo, FOXM1 promoted tumor growth in a subcutaneous xenograft model and lung colonization in a tail-vein injection model. The CUT&Tag sequencing revealed that FOXM1 occupied the tripartite motif containing 59 (TRIM59) promoter, and dual-luciferase reporter assays confirmed that FOXM1 transcriptionally activated TRIM59. Furthermore, FOXM1 gain- and loss-of-function were accompanied by changes in axis inhibition protein 1 (AXIN1) protein levels, β-catenin levels, and β-catenin nuclear translocation, potentially contributing to the regulation of Wnt/β-catenin signaling. Finally, TRIM59 knockdown successfully rescued FOXM1-driven malignant phenotypes. This study identifies a novel FOXM1/TRIM59/Wnt signaling axis that drives hepatoblastoma metastasis, highlighting FOXM1 and TRIM59 as promising therapeutic targets for high-risk patients.