Supplementary Figures 1-19 from ALK-Dependent Control of Hypoxia-Inducible Factors Mediates Tumor Growth and Metastasis

Supplementary Figures 1-19. Supplementary Figure 1. Hypoxia pathways are enriched in ALCL. Supplementary Figure 2. Gene expression data on ALCL. Supplementary Figure 3. EML4-ALK NSCLC show enrichment in hypoxia pathway associated genes. Supplementary Figure 4. ALK regulates HIF-1α and HIF-2α expression in ALK-rearranged ALCL cell lines. Supplementary Figure 5. Oncogenic ALK regulates HIF-1α and HIF-2α expression levels in ALK-rearranged ALCL cell lines. Supplementary Figure 6. Oncogenic ALK-mediated control of HIF-1α and HIF-2α expression is not dependent on proteasome-dependent degradation. Supplementary Figure 7. ALK regulates HIF-1α and HIF-2α through STAT3 and C/EBPβ. Supplementary Figure 8. STAT3 and C/EBPβ mediated regulation of HIFs in ALCL. Supplementary Figure 9. Ectopic expression of NPM-ALK in ALK negative ALCL. Supplementary Figure 10. Validation of shRNA against HIF-1α and HIF-2α. Supplementary Figure 11. HIF-2α is essential for the growth of ALK-rearranged ALCL in vivo. Supplementary Figure 12. HIF-1α and HIF-2α are not required for the growth of ALK-negative T cell lymphoma in vivo. Supplementary Figure 13. ALK regulates VEGFA mRNA expression and production in vitro. Supplementary Figure 14. Anti-angiogenic treatment in ALK negative ALCL. Supplementary Figure 15. Oncogenic ALK regulates HIF-1α and HIF-2α expression levels in EML4-ALK NSCLC. Supplementary Figure 16. HIF-α regulation in NSCLC is specifically dependent on ALK activity. Supplementary Figure 17. Oncogenic ALK activity up-regulates VEGF expression in NSCLC. Supplementary Figure 18. HIF-α knock-down does not affect the growth of K-RAS mutated NSCLC. Supplementary Figure 19. HIF-1α and HIF-2α are essential for metastasis formation in EML4-ALK NSCLC.