Fig. 7: Free iron accumulation is associated with ferroptosis derived from CISD3 knockdown.
From: CISD3 inhibition drives cystine-deprivation induced ferroptosis
A Cell viability assay was monitored in shCISD3 and control cells by CCK8 kit in the presence or absence of indicated molecules (7.5 µM erastin, 100 µM DFO, 0.5 mM GSH, and 10 µM COQ10). B Cell viability of CISD3 silenced cells with or without GPX4 or FTH expression were measured at different concentrations of erastin treatment for 12 h. Long-term cell viability was detected by colony formation assay under the exposure of 0.5 µM erastin for 14 days (C), and corresponding histograms are shown on the right (D). Cell death (E), cellular ROS (F), and cellular lipid peroxides (G) were detected by flow cytometry in indicated cells with or without erastin treatment through Annexin V-PI, DCF-DA, and BODIPY C11 staining, respectively. H The morphological changes of mitochondria were detected by transmission electron microscopy in the absence or presence of 7.5 µM erastin. Lower scale bars: 1 μm. *P < 0.05, **P < 0.01 versus control or between different groups.
