Skip to main content
. 2021 Nov 1;4:1237. doi: 10.1038/s42003-021-02744-4

Fig. 1. EGFR activates YAP/TAZ in HNSCC, independently of PI3K.

Fig. 1

a Immunoblot of pEGFR (Y1068), EGFR, pYAP (S127), YAP, pERK1/2 (T202/Y204), ERK1/2, pAKT (S473), AKT, pS6 (S235/236), S6, CTGF, CYR61, β-actin in CAL33, CAL27, and WSU-HN6. Right panel showing the status of FAT1 gene alterations. b Relative mRNA levels of CTGF, CYR61, and AMOTL2 in CAL33, CAL27, and WSU-HN6 cells. c GSEA analysis of RNA-seq data in CCLE using the C6 oncogenic gene sets, spiked with several previously published YAP-regulated gene sets. NES, normalized enrichment score; NOM, nominal; FDR, false discovery rate. d Immunoblot of pEGFR (Y1068), EGFR, pYAP (S127), YAP, TAZ, pERK1/2 (T202/Y204), ERK1/2, pAKT (S473), AKT, pS6 (S235/236), S6, CTGF, CYR61, β-actin in CAL27 cells. Cells were serum starved for 16 h, and treated with EGF (20 ng/ml) for the indicated time. e Relative mRNA levels of CTGF, CYR61, and AMOTL2 in CAL27 cells. f Immunoblot of pEGFR (Y1068), EGFR, pAKT (S473), AKT, pYAP (S127), YAP, TAZ, CTGF, CYR61, β-actin in CAL27 cells stably overexpressing empty vector or PIK3CA H1047R. Cells were serum starved for 16 h, and treated with EGF (20 ng/ml) for 1 hr. g Immunoblot of pEGFR (Y1068), EGFR, pAKT (S473), AKT, pYAP (S127), YAP, TAZ, CTGF, CYR61, β-actin in CAL27 cells. Cells were serum starved for 16 h, and pretreated with BYL719 (1 μM) for 1 h and followed by EGF treatment (20 ng/ml) for 1 h. ANOVA with Tukey–Kramer post hoc test was used. Mean ± SEM (b, e); ***P  < 0.001; **P < 0.01; *P  < 0.05. *versus CAL33 (b) and versus EGF 0 h (e).