Fig. 10
Integrative model of the eIF4E–Nrf2–ABCB1 axis in doxorubicin resistance. Schematic summary of the proposed mechanism by which sustained eIF4E activation in MDAR cells promotes the selective translation of Nrf2 and ABCB1, enhancing antioxidant response and drug efflux. The convergence of translational control and stress-adaptive signaling reduces intracellular doxorubicin accumulation, thereby reinforcing the chemoresistant phenotype in triple-negative breast cancer cells.
