Abstract
BACKGROUND/AIM: The epidermal growth factor receptor (EGFR) is a key driver in bladder cancer progression. This study investigated the tumor-suppressive role of miR-124-3p and its regulatory effect on EGFR. MATERIALS AND METHODS: TSGH8301 and T24 bladder cancer cells were treated with the EGFR inhibitor erlotinib or transfected with an miR-124-3p mimic. Cell viability, proliferation, migration, and invasion were assessed using MTT, colony formation, and transwell assays. EGFR targeting was confirmed via Western blot, immunofluorescence, and luciferase reporter assays. RESULTS: Erlotinib and miR-124-3p both reduced cell viability and proliferation. miR-124-3p significantly inhibited EGFR phosphorylation and expression, suppressed migration and invasion, and downregulated the EGFR downstream targets MMP2, MMP9, and VEGF-A. Luciferase assays confirmed the direct binding of miR-124-3p to EGFR 3'UTR. CONCLUSION: miR-124-3p suppresses bladder cancer cells progression by directly targeting and inactivating EGFR, thereby impairing cell proliferation, migration, and invasion. These findings highlight miR-124-3p as a potential therapeutic agent in EGFR-driven bladder cancer.