Abstract / Summary
Abstract Objective This study explored how plasma exosomal miR-29b targets FOLR1 and how their interaction with CTNNB1 triggers the Wnt/β-catenin pathway in endometrial cancer (EC). Methods Bioinformatics screening identified differentially expressed genes, candidate targets and upstream regulators, combined with expression and survival analyses. qPCR and western blot detected gene expression in EC and normal tissues/cell lines. qPCR quantified exosomal miR-29b from EC cell culture supernatant and patient plasma. CCK-8, wound healing, Transwell and flow cytometry apoptosis assays assessed cell proliferation, migration, invasion and apoptosis. Dual-luciferase assays verified the direct binding between miR-29b and FOLR1. Co-IP validated FOLR1–CTNNB1 protein interaction. qPCR and western blot detected Wnt pathway molecules after FOLR1 silencing. Nude mouse xenograft models further verified the in vivo functions of FOLR1. Results FOLR1 was confirmed as a direct target of miR-29b. FOLR1 was overexpressed in EC tissues and cells, while miR-29b was markedly downregulated in EC cell-derived and patient plasma exosomes. miR-29b overexpression or FOLR1 knockdown suppressed EC cell proliferation, migration and invasion, and induced apoptosis. miR-29b bound the 3’-UTR of FOLR1 to repress its expression. FOLR1 physically interacted with CTNNB1 to regulate the Wnt/β-catenin cascade. Conclusions Reduced plasma exosomal miR-29b elevates FOLR1, which stabilizes CTNNB1 and activates Wnt/β-catenin signaling to accelerate EC progression. This work reveals a new EC molecular axis and supplies candidate biomarkers for liquid biopsy and therapeutic targets.