Supplementary Figures 1 - 9 from Hedgehog Signaling Alters Reliance on EGF Receptor Signaling and Mediates Anti-EGFR Therapeutic Resistance in Head and Neck Cancer

PDF file - 1255K, Confirmation of GLI1 modulation by EGFR activation (S1); Epithelial gene expression profile and morphology predicts erlotinib sensitivity in HNSCC cell lines (S2); Zeb1 transcription factor is key driver of EGF induced EMT (S3); EGFR activation induces EMT in HNSCC cell lines characterized by expression of Vimentin (S4); Inter-pathway crosstalk as well as EGF induced EMT are blunted in erlotinib resistant cells (S5); Silencing of HhP transcription factor GLI1 increases EGFR driven EMT in Tu-167 cells (S6); MEK/ERK signaling is required for EMT-like state while both MEK/ERK and PI3K/AKT are required for invasion through Matrigel (S7); Proliferative inhibition of erltotinib (1μM and 2μM) plus IPI-926 (1μM) or SHH (250ng/ml) (S8); Cetuximab and IPI-926 modulate EGFR, HhP and EMT gene expression in vivo (S9).