Fig. 7

Schematic model of the mechanism underlying miR-23a-3p on sorafenib resistance in HCC. Sorafenib treatment triggered ferroptosis via lipid ROS production and chelatable iron accumulation. The ETS1 upregulated by sorafenib was a key transcription factor of miR-23a-3p that directly enhanced miR-23a-3p expression. MiR-23a-3p recognized and bound to ACSL4 3’UTR to limit lipid ROS production, thus attenuating sorafenib-induced ferroptotic cell death in HCC