Role of MEX3A in tumorigenesis: Mechanisms, tumor‑specific effects and therapeutic implications (Review).

Muscle excess 3A (MEX3A), a dual‑function RNA‑binding protein with E3 ubiquitin ligase activity, is a pivotal regulator of tumorigenesis. By modulating mRNA stability, translation and targeted protein degradation, MEX3A orchestrates key oncogenic processes, including tumor stemness maintenance, proliferation, migration and immune evasion. MEX3A is aberrantly expressed in various malignancies, such as colorectal and breast cancer, hepatocellular carcinoma and glioblastoma, where it engages key signaling pathways, including the Wnt/β‑catenin, PI3K/AKT and NF‑κB pathways. Mechanistically, MEX3A directly regulates oncogenic and tumor suppressor transcripts, influencing the cell dynamics within the tumor microenvironment. Furthermore, MEX3A upregulation is associated with a poor prognosis and therapy resistance, highlighting its potential as a prognostic biomarker and therapeutic target. The present review aimed to summarize the molecular functions, tumor‑specific roles and translational relevance of MEX3A, bridging the gap between mechanistic insight and clinical applications. Future studies exploring MEX3A‑targeted interventions may reveal novel strategies for precision oncology.