Supplemental Figures S1-S11, Datasets 1-3 from AXL Inhibition Sensitizes Mesenchymal Cancer Cells to Antimitotic Drugs

Supplemental Figures S1-S11. Figure S1. AXL and GAS6 expression correlates with a mesenchymal signature. Figure S2. AXL staining in TNBC tissues samples. Figure S3. TGF-β-induced EMT is reversible, and TKI resistance upon EMT is not due to drug efflux. Figure S4. AXL inhibitor R428 suppresses GAS6-induced pAXL, downstream signaling and invasion capacity. Figure S5: Inhibition of AXL does not re-sensitize erlotinib-resistant cells. Figure S6: AXL over-expression or inhibition does not alter erlotinib sensitivity in the parental HCC827 cell line. Figure S7: Summary of Bliss scores and activity of MP-470, Erlotinib and Docetaxel (DTX) or combination treatment. Figure S8. R428 synergistically interacts with anti-mitotic agents and not with Doxorubicin or Cisplatin to reduce cell viability. Figure S9. AXL inhibition in combination with anti-mitotic agents promotes mitotic death. Figure S10. Suppression of pAKT, pS6 and pCDC2 following AXL inhibition. Figure S11: AXL knock-down increases p21 expression. Table S1. Mesenchymal PC9 cells are cross-resistant to a number of anti-cancer agents.