Supplementary Data from Inhibiting BRAF Oncogene–Mediated Radioresistance Effectively Radiosensitizes BRAFV600E-Mutant Thyroid Cancer Cells by Constraining DNA Double-Strand Break Repair

Supplementary Table 1. Thyroid cancer cells lines used in this study Supplementary Figure 1. AlamarBlue® proliferation assay of TPC-1 stable cell lines. Supplemental Figure 2. Assessment of MEK-ERK activation in TPC-1 BRAFV600E stable cells. Supplementary Figure 3. Pooled radiation sensitivity data from melanoma, thyroid, colorectal cell lines either with BRAFV600E mutation or not. Supplementary Figure 4. Representative photos of plates from radiation clonogenic assays showing the effects of BRAFV600E inhibition with vemurafenib (Vem) resulting in radiosensitization in thyroid cancer cells harboring a BRAFV600E mutation (8505C, BCPAP) compared to vehicle (Ctrl) treated cells. Supplementary Figure 5. Plating efficiency of various thyroid cancer cell lines during radiation clonogenic assays in the presence of vemurafenib (Vem, 100nM) or vehicle (Ctrl). Supplementary Figure 6. BRAFV600E inhibition radiosensitizes melanoma cancer cells harboring a BRAFV600E mutation. Supplementary Figure 7. BRAFV600E inhibition does not alter the recovery of IR-induced DNA damage in BRAFWT thyroid cancer cells. Supplemental Figure 8. Assessment of BRAFV600E expression and MEK-ERK activation in 293T cells. Supplemental Table 2. mRNA expression ratio of NHEJ associated genes of thyroid cancer with BRAFV600E mutation compared to BRAF wild-type (BRAF wild-type: 203 cases; BRAFV600E mutant: 288 cases). Supplementary Figure 9. Expression of XLF is sufficient to induce radioresistance. Supplementary Figure 10. Treatment of BRAF inhibitor did not lead to significant weight loss of mice.