Additional file 1 of A transcriptomic map of EGFR-induced epithelial-to-mesenchymal transition identifies prognostic and therapeutic targets for head and neck cancer

Additional file 1: SupplementaryFigure 1. Copy number variation and expression of EGFR in Kyse30and FaDu cells. Supplementary Figure 2. GSEA of EGF- and EpEX-treated Kyse30and FaDu cells. Supplementary Figure 3. Over-representation analysis of genesof the EGFR-mediated EMT signature. SupplementaryFigure 4. Comparison ofEGFR-mediated EMT, pEMT, and EMT signatures. Supplementary Figure 5. Comparisonof EMT signatures for prognostic purposes.Supplementary Figure 6. ITGB4,ITGA6, LAMA3, LAMB3, and LAMC2 expression in HNSCC. Supplementary Figure 7. ITGB4expression in malignant and non-malignant single cells in different cancerentities. Supplementary Figure 8. ITGA6 expression in malignant andnon-malignant single cells in different cancer entities. Supplementary Figure 9. LAMA3expression in malignant and non-malignant single cells in different cancerentities. Supplementary Figure 10. LAMB3 expression in malignant andnon-malignant single cells in different cancer entities. Supplementary Figure 11. LAMC2expression in malignant and non-malignant single cells in different cancerentities. Supplementary Figure 12. ITGB4 expression in knockdown clonesof Kyse30 and FaDu cells. Supplementary Figure 13. Wound healing capacity of control andITGB4-knockdown cell lines. SupplementaryFigure 14. Tumor buddingintensities in HNSCC

Additional file 4 of A transcriptomic map of EGFR-induced epithelial-to-mesenchymal transition identifies prognostic and therapeutic targets for head and neck cancer

Additional file 4: Supplementary Table 3. Gene expression correlation with ITGB4 in the HPV-negativeTCGA cohort. Batch correlation analysis identified correlations of geneexpression with integrin beta 4 (ITGB4). Gene ID, Spearman correlation, andp-value are indicated for the top ten positively (co-regulated) and negativelycorrelated genes (counterregulated)

Additional file 3 of A transcriptomic map of EGFR-induced epithelial-to-mesenchymal transition identifies prognostic and therapeutic targets for head and neck cancer

Additional file 3: Supplementary Table 2. TCGA HPV- HNSC cohort

Additional file 2 of A transcriptomic map of EGFR-induced epithelial-to-mesenchymal transition identifies prognostic and therapeutic targets for head and neck cancer

Additional file 2: Supplementary Table 1. EGFR-mediated EMT

Additional file 5 of A transcriptomic map of EGFR-induced epithelial-to-mesenchymal transition identifies prognostic and therapeutic targets for head and neck cancer

Additional file 5: Supplementary Table 4. SCC1 cell line: DEGs overlapping with EGFR-mediated EMT signature

Additional file 5 of Tumor cell integrin β4 and tumor stroma E-/P-selectin cooperatively regulate tumor growth in vivo

Additional file 5. Suppl. Fig. S5: Attraction of human macrophages by ITGB4 knockdown tumor cell-conditioned media. Entire dataset of data shown in Fig. 7A including further donors

Additional file 3 of Tumor cell integrin β4 and tumor stroma E-/P-selectin cooperatively regulate tumor growth in vivo

Additional file 3. Suppl. Fig. S3: Western Blot analyses of PC-3 xenograft tumor samples. Exemplary Western Blot images and corresponding quantification of cell cycle- and survival-related protein levels relative to HSC70. Proteins were extracted from PC-3 xenograft tumors from the experiment shown in Fig. 1D. The combination group (shITGB4/KO) is missing since in this group only one mouse developed a xenograft tumor. Bar charts represent mean+SD of n=5. *p<0.05; **p<0.01

Additional file 2 of Tumor cell integrin β4 and tumor stroma E-/P-selectin cooperatively regulate tumor growth in vivo

Additional file 2. Suppl. Fig. S2: Cox proportional hazards regression model including cell line and KD condition as predictors to obtain cell line-adjusted effects of the ITGB4 knockdown condition on mouse survival (experiments shown in Figs. 1D, Fig. 2A and 3A)

Additional file 4 of Tumor cell integrin β4 and tumor stroma E-/P-selectin cooperatively regulate tumor growth in vivo

Additional file 4. Suppl. Fig. S4: Enhanced attraction of tumor-infiltrating leukocytes in ITGB4-depleted xenografts. Morphology of control and ITGB4 KD tumors in WT and KO mice based on HE stainings (A). Arginase-1, myeloperoxidase (MPO) and inducible nitric oxide synthase (iNOS) expression in control vs. ITGB4 KD PC-3 tumor nodules on d8 after engraftment (B). Intraperitoneal (IP) carcinosis score (ICS) on day 49 after injection of SKOV3 control vs. ITGB4 knockdown cells into E-/P-selectin wildtype vs. knockout rag2-/- BALB/c mice. Representative anti-mCD45 immunostaining images of formalin-fixed, paraffin-embedded intraperitoneal lavage (C). Black lines in the scatter plot represent mean values. **p<0.01; ***p<0.001

Additional file 10 of Tumor cell integrin β4 and tumor stroma E-/P-selectin cooperatively regulate tumor growth in vivo

Additional file 10. Suppl. Table 1: Short IHC protocols relevant to the study (IHC-P)