Figure 5: TEAD4-S can inhibit tumour growth in vivo.

(a) H157 cells stably expressing YAP, YAP/TEAD4-FL, YAP/TEAD4-S, YAP/RBM4 or vector control were subcutaneously injected into the flank of nude mice. Each group contained nine mice. Pictures of the tumours removed after 17 days were shown. Scale bar, 1 cm. (b) The growth of xenograft tumours was monitored and the average sizes of xenograft tumours were measured every 2 days (n=9, error bars indicate±s.d., P<0.05 by t-test). (c) Total RNA isolated from seven paired NSCLC tumours and adjacent normal tissues were assayed by semi-quantitative RT–PCR. The mean±s.d. from three experiments was plotted. (d) TEAD4 levels from seven paired NSCLC tumours and adjacent normal tissues were analysed by western blot. (e) The splicing alteration of TEAD4 was examined in various cancers by analysing the TCGA consortium containing RNA-seq data sets from thousands of patients. The PSI of TEAD4 in the cancer or normal samples are presented as standard box plot, with the boxes presenting the first and third quartiles and the whiskers representing the 2nd and 98th percentiles. ***P< 0.0005; **P< 0.005; *P< 0.05; and NS, not significant. (f) The overall survivals of lung cancer and colon cancer patients with different ratios of TEAD4 splicing isoforms were analysed. (g) The model of how the Hippo–YAP pathway is regulated through a TEAD4 splicing switch.