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Fig. 1 | Molecular Cancer

Fig. 1

From: Resistance of HNSCC cell models to pan-FGFR inhibition depends on the EMT phenotype associating with clinical outcome

Fig. 1

RNAi cell viability screen identifies FGF-receptors as potent cytotoxic and radiosensitizing targets for HNSCC cell models with and without simultaneous β1 integrin targeting. A Gene expression analysis of 10 selected, clinically relevant RTK with available FDA-approved drugs (Table S2) in HPV-negative HNSCC patients of the TCGA cohort. Data of normalized primary tumor (n = 415) and normal tissues (n = 44) were compared using unpaired t test (***p ≤ 0.001, **p ≤ 0.01). B OncoPrint of target gene alterations in HPV-negative HNSCC patients of the TCGA cohort (n = 415). Percentage indicates the proportion of patients with genetic alterations. Only data of patients with alterations are shown. C Workflow of RNAi cell viability screen in 3D lrECM (laminin-rich extracellular matrix) HNSCC cell models. Images were partly adapted from Servier Medical Art by Servier, licensed under a Creative Commons Attribution 3.0 Unported License. D Enhancement ratios (ER) of cell viability of 3D lrECM HNSCC models upon single or double siRNA-mediated knockdowns of 10 RTK and β1 integrin (labeled as β1). ER and statistics are derived from corresponding cell viability data (Fig. S2A) and presented as mean ± range (n = 3; two-way ANOVA; Dunnett’s multiple comparison test to corresponding controls). E ER of cell viability of 6 Gy X-ray irradiated 3D lrECM HNSCC models upon single or double knockdowns of 10 RTK and β1 integrin. ER and statistics are derived from the corresponding cell viability data (Fig. S2B) and presented as mean ± range (n = 3; two-way ANOVA; Dunnett’s multiple comparison test to corresponding irradiated controls)

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