Fig. 2: DCAF7 deficiency induces ferroptosis to suppress HCC progression through the HIF1α-SLC7A11 axis.

A and B The relative cell viability of siNC or siDCAF7-transfected Huh7 cells treated with different concentrations of the ferroptosis inducer Erastin (A) or RSL3 (B) for 24 h. Mean ± SD (n = 3, biological replicates). C and D The OD450 of siNC or siDCAF7-transfected HCC cells treated with DMSO or Fer-1 (1 μM) for different durations. Mean ± SD (n = 3, biological replicates). E–G The relative intracellular GSH (E), ROS (F), and MDA (G) levels for the control or DCAF7-knockdown HCC cells. Mean ± SD (n = 3, biological replicates). H qPCR analysis of ferroptosis-related genes in the control or DCAF7-knockdown HepG2 and SMMC-7721 cells. I Western blotting analysis of SLC7A11 in the control or DCAF7-knockdown HCC cells. Mean ± SD (n = 3, biological replicates). J–L The relative intracellular GSH (J), ROS (K), and MDA (L) levels in the control or DCAF7-knockdown Huh7 and SNU-449 cells transfected with an empty vector or HA-SLC7A11 plasmid. Mean ± SD (n = 3, biological replicates). M Western blotting analysis of HIF1α and SLC7A11 in the control or DCAF7-knockdown HCC cells. Mean ± SD (n = 3, biological replicates). N–P qPCR and Western blotting analysis of the relative mRNA (N and O) and protein level (P) of SLC7A11 in the control or DCAF7-knockdown HCC cells transfected with an empty vector or HA-HIF1α plasmid. Mean ± SD (n = 3, biological replicates). Q–S The relative intracellular GSH (Q), ROS (R), and MDA (S) levels for the control or DCAF7-knockdown Huh7 and SNU-449 cells transfected with an empty vector or HA-HIF1α plasmid. Mean ± SD (n = 3, biological replicates). The P-values were calculated using two-tailed, unpaired Student’s t-test (E–G, I, and M), one-way ANOVA analysis with a Tukey’s multiple comparisons post hoc test (J–L, and N–S), and two-way ANOVA analysis with a Sidak’s multiple comparisons post hoc test (A–D). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.