Fig. 3: URI alleviated TKI-induced ferroptosis in a SCD1-dependent manner.

a Western blotting (WB) of certain lipid metabolism associated enzymes in HepG2 cells infected with lentivirus containing control or two URI-shRNA sequences, respectively. The relative intensities of WB bands were normalized to GAPDH. Three experiments were performed and the representative images from one experiment were shown. b Relative viability of cells treated with 10 μM sorafenib in the presence and absence of A939572 (10μM), MK8245 (10 μM), or Ferrostatin-1 (20 μM) for 48 h (n = 3 biological replicates). c, d Long-term colony-formation assay of cells treated with 2.5 μM sorafenib (Sora) in the presence and absence of A939572 (A, 2.5 μM), MK8245 (M, 2.5 μM), or Ferrostatin-1 (F, 5 μM) for 14 days (c), and the quantification of three independent assays was shown in (d). e Liperfluo assays of JHH1 and HepG2 cells with or without URI knockdown treated with 10 μM sorafenib in the presence and absence of A939572 (10 μM), MK8245 (10 μM), or Ferrostatin-1 (20μM) for 48 h (n = 3 biological replicates). f JHH1-Ctrl, JHH1-shURI, HepG2-Ctrl, and HepG2-shURI cells were transfected with MOCK or Flag-SCD1 plasmids for 48 h and then treated with 10 μM sorafenib, the relative viability of cells was measured (n = 3 biological replicates). g HepG2-Ctrl and HepG2-shURI cells transfected with MOCK or Flag-SCD1 plasmids were treated with 10μM sorafenib in the presence and absence of A939572 (10 μM) or MK8245 (10 μM) for 48 h and the lipid peroxidation was measured (n = 3 biological replicates). Data are means ± SEM. Statistical significance in (b) and (d–g) is determined by two-tailed unpaired t-test. Source data are provided as a Source Data file.