Our study identifies EIF4A3 as a critical post-transcriptional regulator and downstream effector of the TGF-β/SMAD pathway. EIF4A3 forms a positive feedback loop with TGF-β/SMAD signaling, thereby reinforcing EMT and promoting metastatic progression in GC. These findings establish EIF4A3 as a novel post-transcriptional amplifier of TGF-β signaling and a promising candidate for diagnostic and therapeutic intervention in metastatic GC.
Liu et al. (Fri,) studied this question.