Fig. 5: Iron homeostasis is dysregulated in therapy-induced senescent HGSOC cells.
From: Exploiting dysregulated iron homeostasis to eradicate persistent high-grade serous ovarian cancer
A Heatmaps of most commonly differentially regulated proteins from proteomics analysis of OVCAR3, OVCAR4, OVCAR8, AOCS14 and AOCS30 cells exposed to cisplatin or CX-5461 and their respective vehicle controls, as determined by number of drug-treated vs. control samples showing fold change > 1.5 or < −1.5. B Quantification of FTH1 protein abundance from n = 4 independent experiments is shown as mean ± SD. C Western blots of FTH1 protein expression. Actin was probed as a loading control. D Quantification of total iron content from ICP-MS analysis of OVCAR3, OVCAR4 and OVCAR8 cells exposed to cisplatin or CX-5461 and their respective vehicle controls is shown as mean ± SEM from n = 4 replicates. Statistical analysis was performed using one-way ANOVA with a Šídák’s multiple comparisons test. **p < 0.01; ***p < 0.001; ****p < 0.0001; ns not significant. E Quantification of free labile iron as measured by FerroOrange median fluorescence intensity is shown as mean ± SD from n = 3 replicates. Statistical analysis was performed using one-way ANOVA with a Šídák’s multiple comparisons test. ***p < 0.001; ****p < 0.0001. F Representative Western blots of key regulators of iron homeostasis. Actin was probed as a loading control.
