Extended Data Fig. 3: SCRN1 enhances tumor resistance to ferroptosis.
a, Expression and phosphorylation of indicated molecules in WT and SCRN1 KO HepG2 cells after sorafenib treatment. b, Expression of indicated molecules in WT and SCRN1 KO HepG2 cells. c, Cell death of WT and SCRN1 KO HepG2 cells pre-treated with different cell death inhibitors and stimulated with sorafenib. d-f, Lipid peroxidation (d), C11-BODIPY fluorescence (e) and representative images of Fe2+ content (f) of WT and SCRN1 KO HepG2 cells stimulated with sorafenib (n = 3 biological replicates). Gating strategy for C11-BODIPY fluorescence was presented in the upper panels of corresponding figures (e). g, Establishment of stably SCRN1 OE Huh7 cells. h, i, Percentage of cell death (h) and C11-BODIPY fluorescence (i) of WT and SCRN1 OE Huh7 cells treated with sorafenib and erastin (n = 3 biological replicates). j, k, Percentage of cell death (j) and C11-BODIPY fluorescence (k) of Hep3B cells transfected with control or SCRN1 siRNA and treated as indicated (n = 3 biological replicates). l, Establishment of stably SCRN1 KO HT1080 and NIH3T3 cells. m-p, Percentage of cell death (m, o) and C11-BODIPY fluorescence (n, p) of WT and SCRN1 KO HT1080 and NIH3T3 cells treated with indicated FINs (n = 3 biological replicates). q, Establishment of stably SCRN1 OE HT1080 and NIH3T3 cells. r-u, Percentage of cell death (r, t) and C11-BODIPY fluorescence (s, u) of WT and SCRN1 OE HT1080 and NIH3T3 cells treated with sorafenib and erastin (n = 3 biological replicates). v-y, Percentage of cell death (v, x) and C11-BODIPY fluorescence (w, y) of HCT116 and SW480 cells transfected with control or SCRN1 siRNA and treated as indicated (n = 3 biological replicates). Data shown are representative of three independent experiments with similar results (a, b, g, l, q). Data presented as mean ± s.d. of three independent experiments and statistical significance was determined by two-tailed unpaired Student’s t-test (d, e, h-k, m-p, r-y).