Tubacin induces TFEB-dependent ferritinophagy independently of HDAC6 and sensitizes cancer cells to ferroptosis under GSH-GPX4 axis disruption.
These findings identify TFEB-driven lysosomal activation and ferritinophagy as a critical determinant of ferroptotic sensitivity under redox imbalance and suggest that pharmacological modulation of TFEB-lysosomal function by tubacin may represent a potential strategy for enhancing ferroptosis-based cancer therapy.