Skip to main content
. Author manuscript; available in PMC: 2023 Mar 2.
Published in final edited form as: Mol Cancer Res. 2022 Sep 2;20(9):1429–1442. doi: 10.1158/1541-7786.MCR-22-0085

Figure 2: Ferroptosis as mediator for CERK inhibition-induced cell death.

Figure 2:

(A-E) A549 cells (LUAD) were pretreated with vehicle (Veh) or pan caspase inhibitor Z-vad-fmk (Z-vad, 25 μM) (A, B), necrosis inhibitor Necrostatin-1 (Nec-1, 10 μM) (C), autophagy inhibitor Chloroquine (CQ, 10 μM) (D), ferroptosis inhibitor Ferrostatin-1 (Fer-1, 5 μM) or iron-chelator deferoxamine (DF, 100 μM) (E) for 1 hour then treated with Veh, NVP-231 (400 nM) or Cisplatin (Cis; 1 μM except in panel B as labeled) for additional 16 hours before cells were utilized in clonogenic survival assay or Western immunoblotting. (F, G) Protein lysate from A549 cells treated with Veh or Fer-1 (5 μM) followed by 16 hours of Veh or NVP-231 (400 nM) treatment were subjected to lipid peroxidation (MDA) assay (F) or Western immunoblotting (G). Data in graphs are means ± SD; n = 6-7 in (A, C-F) or n=4 in (G) from two independent occasions. #p<0.01, ##p<0.001, *p<0.00005, **p<0.000005. Unless otherwise noted by an * or depicted p-value, data are not significant (NS) between depicted groups; p>0.05.