Extended Data Fig. 2: FSP1’s anti-ferroptotic function is not dependent on oncogenic signalling.
a, FSP1 (AIFM2) expression of KRAS-mutant primary LUAD tumours from TCGA, divided into early and late tumour stages (normal lung, n = 54; stage I/II, n = 354; III/IV, n = 98). b, FSP1 (AIFM2) expression of KRAS-mutant primary LUAD tumours from TCGA, separated by the KRAS mutation (G12C n = 51; G12V n = 32; G12D n = 17; G12A n = 16; other n = 20). c, FSP1 (AIFM2) expression of primary LUAD tumours from TCGA, separated by oncogenic driver mutation (normal lung, n = 59; EGFR, n = 71; KRAS, n = 135; other n = 307). d, Western blot of KP LUAD human cell lines treated with 50 nM RMC-042 for indicated durations. e, representative multi-IF images of KP tumours for markers indicated. Panels are 10X, scale bars: 50 µm; insets are 20X, scale bars: 20 µm. f, FSP1 (AIFM2) expression of KRAS-mutant primary LUAD tumours from TCGA, separated by tumour co-mutation status (KEAP1/STK11 WT n = 88; STK11 mutant n = 20; KEAP1 mutant n = 16; KEAP1/STK11 mutant n = 11). g, FSP1 (AIFM2) expression in KP LUAD human cell lines treated with an Nrf2 activator, KI696, for 5 days (n = 3 per group). Box plots indicate median (middle line), 25th, 75th percentile (box) and 5th and 95th percentile (whiskers). Data are represented as mean values, error bars represent SEM, significance determined via one-way ANOVA with multiple comparisons (panels a–c, f, g). For gel source data, see Supplementary Data 1.
