Fig. 6: S100P-ACC1 axis is an alternative pathway to regulate ferroptosis sensitivity.

a Cell death measurements of HuH7 WT and S100P KO cells pretreated with PF-05175157 (50 nM) for 12 h and followed by RSL3 (2 µM) treatment for 6 h. b Cell death measurements of HepG2 WT and S100P KO cells pretreated with PF-05175157 (50 nM) for 12 h and then RSL3 (2 µM) treatment for 6 h. c Cell death measurements of SNU387 and S100P OE cells pretreated with PF-05175157 (25 nM) for 12 h and then RSL3 (200 nM) treatment for 6 h. d Cell death measurements of HT1080 and S100P OE cells pretreated with PF-05175157 (100 nM) for 12 h and then RSL3 (200 nM) treatment for 6 h. e Western blot analysis in S100P KO cells of HuH7 expressing sg-ctrl and sg-ACC1. f Cell death measurements of HuH7 KO cells expressing sg-ctrl or sg-ACC1 treated with RSL3 (2 µM) for 6 h. g Western blot analysis of SNU387 cells expressing sg-ctrl and sg-ACC1. h Cell viability assay of SNU387 cells expressing sg-ctrl or sg-ACC1 treated with RSL3 (200 nM) for 6 h. i Cell death measurements of SNU387 cells expressing sg-ctrl or sg-ACC1 treated with RSL3 (200 nM) for 6 h. j Western blot analysis of HT1080 cells expressing sg-ACC1. k Cell viability assay of HT1080 cells expressing sg-ctrl or sg-ACC1 treated with RSL3 (200 nM) for 6 h. l Cell death measurements of HT1080 cells expressing sg-ctrl or sg-ACC1 treated with RSL3 (200 nM) for 6 h. m Lipid peroxidation measurements of S100P KO cells treated with RSL3 (1 µM) and lipro-1 (2 µM) for 6 h after knockout of ACC1. The Western blot experiments were repeated three times independently with similar results in e, g and j. Data and error bars are mean ± s.d., n =  3 biological independent experiments in a–d, f, h, i and k–m. Statistical analysis was done with two-tailed Student’s t test. Source data are provided as a Source Data file.