Fig. 5: PNO1 inhibition enhances vulnerability of the ferroptosis induced by sorafenib.

A, B Cell viability was assayed in Hep3B sh-PNO1 cells (A) and HLE cells (B) treated with or without sorafenib (0–10 μM) for 24 h controlled with their parental cells (***P < 0.001). C, D Cell viability was assayed in indicated Hep3B (C) and HLE (D) cells treated with or without sorafenib (5 μM for Hep3B, 10 μM for HLE) and ferrostatin-1 (5 μM) for 24 h (***P < 0.001). E, F Cell death was assayed in indicated Hep3B (E) and HLE (F) cells treated with or without sorafenib (5 μM for Hep3B, 10 μM for HLE) and ferrostatin-1 (5 μM) for 24 h (***P < 0.001). G, H The lipid ROS levels were assayed in indicated Hep3B (G) and HLE (H) cells treated with or without sorafenib (5 μM for Hep3B, 10 μM for HLE) for 24 h (**P < 0.01, ***P < 0.001, *P < 0.05). I, J The relative GSH levels were measured in indicated Hep3B (I) and HLE (J) cells treated with or without sorafenib (5 μM for Hep3B, 10 μM for HLE) for 24 h (***P < 0.001).