Additional file 1 of Dual targeting of BRAFV600E and ferroptosis results in synergistic anticancer activity via iron overload and enhanced oxidative stress

Supplementary Material 1. Fig S1. Erastin treatment of ATC cell lines. Fig S2. Effect of dabrafenib and RSL3 combination on the MEK pathway. Fig S3. Ferroptosis inhibition reverses the growth-suppressive effects of C18 alone and C18 combined with dabrafenib in BRAFV600E-mutant ATC cells. Ferrostatin-1 (2 µM) and liproxstatin-1 (2 µM) are ferroptosis inhibitors that block lipid peroxidation. ATC cells were treated with C18 (25 nM), dabrafenib (5 µM), ferrostatin-1 (2 µM), or liproxstatin-1 (2 µM) for 48 h. Proliferation was measured using the CyQUANT Cell Proliferation Assay. (A) The reduction in cell proliferation caused by C18 treatment is rescued by co-treatment with ferrostatin-1 or liproxstatin-1. (B) The antiproliferative effect of combined C18 and dabrafenib is similarly reversed by ferrostatin-1 or liproxstatin-1. Statistical analysis was performed using one-way ANOVA in GraphPad Prism. Significance: *P < 0.05; **P < 0.01; ***P < 0.001; ns = nonsignificant. Fig S4. Representative bioluminescence images of mice depicting tumor luciferase intensity at 14 days post-treatment. Table S1. Dabrafenib (D) and RSL3 (R) combination shows synergistic activity on BRAFV600E-mutant thyroid cancer cells. Table S2. The list of primary and secondary antibodies used in the study.