EIF3B promotes oral squamous cell carcinoma progression via the PI3K/AKT pathway and is negatively regulated by miR-124-3p.

Oral squamous cell carcinoma (OSCC) has a poor prognosis and lacks effective therapeutic targets. Eukaryotic initiation factor 3B (EIF3B) is aberrantly overexpressed in multiple cancers, yet its role in OSCC remains unclear. Bioinformatic analyses identified EIF3B as a potential target of the tumor-suppressive microRNA miR-124-3p. In this study, the expression of miR-124-3p and EIF3B was examined in OSCC tissues and cell lines by qRT-PCR and western blotting, and their direct interaction was verified using a dual-luciferase assay. Functional effects on proliferation, migration, apoptosis, and tumorigenicity were evaluated through in vitro and xenograft assays. The underlying mechanisms were explored via analysis of PI3K/AKT signaling and epithelial-mesenchymal transition (EMT) markers, with LY294002 used to confirm pathway dependency. EIF3B was significantly upregulated, while miR-124-3p was downregulated, in OSCC tissues (n = 49). EIF3B expression correlated with advanced TNM stage and poor prognosis. EIF3B promoted proliferation, migration, and invasion, and inhibited apoptosis, whereas miR-124-3p exerted the opposite effects. miR-124-3p directly targeted the 3'UTR of EIF3B, and EIF3B overexpression reversed its suppressive effects. EIF3B activated PI3K/AKT signaling and EMT, both of which were abolished by miR-124-3p or LY294002. These findings define the miR-124-3p/EIF3B/PI3K-AKT axis as a key regulator of OSCC progression and suggest EIF3B as a potential prognostic biomarker and therapeutic target.