Supplemental Data from <i>NRAS</i>-Mutated Rhabdomyosarcoma Cells Are Vulnerable to Mitochondrial Apoptosis Induced by Coinhibition of MEK and PI3K<b>α</b>

Suppl. Figure 1. NRAS depletion reduces cell viability of NRAS mutated RMS cells. Suppl. Figure 2. MEK162 and BYL719 synergize to induce apoptosis in NRAS-mutated RMS cells. Suppl. Figure 3. MEK162 and BYL719 synergize to induce apoptosis in NRAS-mutated neuroblastoma and leukemia cell lines. Suppl. Figure 4. MEK162/BYL719-induced caspase-dependent apoptosis. Suppl. Figure 5. Effect of NRAS knockdown on RAF/MEK/ERK and PI3K/AKT/mTOR signaling. Suppl. Figure 6. Effect of MEK162/BYL719 cotreatment in RAS wildtype RMS cells. Suppl. Figure 7. NRAS knockdown induces BIM and BMF mRNA expression. Suppl. Figure 8. NRAS silencing is synthetic lethal with MCL-1 inhibition. Suppl. Figure 9. Expression of BIM, BMF and MCL-1 in RMS cell lines. Suppl. Figure 10. MEK162/BYL719 cotreatment increases the binding of BMF and BIM to antiapoptotic BCL-2 proteins. Suppl. Figure 11. MEK162 and BYL719 cooperate to trigger BAX and BAK activation. Suppl. Table 1. List of primers Suppl. Table 2. Summary of identified RAS mutations in RMS cell lines. Suppl. Table 3. Synergistic induction of apoptosis by MEK162 and BYL719.