Fig. 5

SNORA56 causes GCLC-mediated CRC ferroptosis resistance and proliferation. (A, C, S, X, Q) HCT116, HCT8, HT29, and HIEC cells were transfected as indicated, stained with the BODIPY C11 probe, and subjected to flow cytometry for lipid ROS detection. (B, D, T, Y, R) HCT116, HCT8, HT29, and HIEC cells were subjected to indicated transfections, followed by propidium iodide staining and cell death analysis using flow cytometry. (E) The relative Fe²⁺/Fe³⁺ ratios in HT29 and HIEC cells after indicated transfections. (F) The relative GSH/GSSG ratios in HT29 and HIEC cells after indicated transfections. (G-J) Lipid ROS levels and cell death in HCT116 and HCT8 cells transfected with SNORA56 ASOs and control ASO, followed by treatment with DMSO, Fer-1, necrosulfonamide, and Z-VAD-FMK, were measured using flow cytometry. (K-L) The cell viability of HT29 and HIEC cells after indicated transfections and treatment with various erastin concentrations for 24 h, was determined using the CCK8 assay. (M) A schematic representation of GSH synthesis. (N, U) GCL enzyme activity in HT29 and HIEC cells after indicated treatment. (O-P, V-W) CCK8 and colony formation assays were used to assess the proliferation of treated HT29 and HIEC cells