Fig. 5

TEAD4 knockdown inhibits cell proliferation, migration and invasion, and triggers apoptosis in HNSCC cells. a Endogenous TEAD4 protein expression was measured in a panel of HNSCC cell lines as compared to normal oral epithelial (HOK). Representative images of western blot (WB) were shown from 3 independent experiments. b Endogenous TEAD4 was efficiently silenced by 2 siRNAs (siTEAD4–1, siTEAD4–2) in Cal27 and Fadu cells. Non-targeting siRNA was utilized as negative control (siNC). Representative images of WB are shown from 3 independent experiments. c Cell proliferation was remarkably suppressed when endogenous TEAD4 was silenced as measured by CCK-8 viability assay. d The potentials of colony formation were significantly inhibited in TEAD4-depleted cells (transfected with siTEAD4–1) as compared to control (siNC). e, f Increased percentages of cell undergoing apoptosis were evident following TEAD4 knockdown as assayed by Annexin V-PI staining. g–i The migration (g) and invasion (h) abilities were significantly reduced in siTEAD4-transfected cells in wound healing (12, 24 h after cell scratching) and transwell assays (12 h after cell seeding), respectively. Scale bar: 100 μm. Quantitive data of transwell assays were shown in i. Data shown here are mean ± SD from three independent experiments, *P < 0.05, **P < 0.01, ANOVA analyses with Tukey’s multiple comparisons test