Fig 1: Apatinib disrupted redox balance and mitochondrial function to suppress lung CSC-like properties.a Protein levels of NOX4, NQO1, SOD2, and GPX4 in A549 and H1299 cells after various concentrations of apatinib treatment. One-way ANOVA (Bonferroni’s multiple-comparison test) was used. Data are presented as mean ± SD (n = 3). *p < 0.05, **p < 0.01 compared to the control group. b Protein levels of NOX4, NQO1, SOD2, and GPX4 in apatinib (5 µM)-treated cells treated with/without 5 mM NAC or 200 µM H2O2 for 48 h. One-way ANOVA (Bonferroni’s multiple-comparison test) was used. Data are presented as mean ± SD (n = 3). *p < 0.05, **p < 0.01 compared to the control group; #p < 0.05, ##p < 0.01 compared to the apatinib (5 µM) group. c Immunofluorescence analysis of JC-1 in cells after various concentrations of apatinib treatment for 24 h. Scale bar = 25 µm. One-way ANOVA (Bonferroni’s multiple-comparison test) was used. Data are presented as mean ± SD (n = 3). **p < 0.01 compared to the control group. d Immunofluorescence analysis of ?H2AX (red) in apatinib (1 µM) -treated cells with/without 5 mM NAC or 200 µM H2O2. DAPI: blue. Scale bar = 100 µm. e Sphere formation assays of apatinib (1 µM)-treated with/without 5 mM NAC or 200 µM H2O2. Scale bar = 100 µm. One-way ANOVA (Bonferroni’s multiple-comparison test) was used. Data are presented as mean ± SD (n = 3). *p < 0.05, **p < 0.01 compared to the control group; #p < 0.05, ##p < 0.01 compared to the apatinib (1 µM) group. f Protein levels of ALDH1A1 and ABCG2 in apatinib (5 µM) treated with/without 5 mM NAC or 200 µM H2O2 48 h. One-way ANOVA (Bonferroni’s multiple-comparison test) was used. Data are presented as mean ± SD (n = 3). *p < 0.05, **p < 0.01 compared to the control group; ##p < 0.01 compared with the apatinib (5 µM) group. g Schematic representation of the effects of apatinib on lung CSC-like properties by inducing redox imbalance.