Fig. 5: TEAD–YAP blockade activates AKT activity through PIK3C2B and SOX4.
From: Pharmacological blockade of TEAD–YAP reveals its therapeutic limitation in cancer cells
a Immunoblot of p-AKT (T308), p-AKT (S473) and total AKT in Huh7, DLD1, HCT116, HCT15, H226 and H1299 cells treated with MGH-CP1 at indicated time point. b Immunoblot of p-AKT (S473) and total AKT in DLD1 and HCT116 cells treated with TEAD-YAP inhibitors, including celastrol, TEAD347 and CIL56 at indicated time point. c DLD1 and HCT116 cells were treated with either of MGH-CP1, pan-PI3K inhibitor Wortmannin, or combination. p-AKT (S473) and total AKT levels were determined by immunoblot. a–c Representative images were chosen from n = 3 biological repeats. d DLD1 cells were transfected with sets of SOX2 siRNAs, followed by MGH-CP1 treatment for 24 h, p-AKT (T308), p-AKT (S473) and total AKT were examined by immunoblot. SOX4 expression levels were evaluated by qPCR after SOX4 siRNA knockdown (n = 3 biological repeats). Huh7 (e) and HCT116 (f) cells were overexpressed with SOX4 or PIK3C2B in the presence of MGH-CP1. Cell viability was shown at different concentrations (n = 3 biological repeats). Huh7 (g) and HCT116 (h) cells were treated with control siRNA and SOX4/PIK3C2B siRNA. Cell viability with treatment of different concentration of MGH-CP1was determined (n = 3 biological repeats). Data are represented as mean ± S.E.M. P values were determined using two-tailed t-tests. Source data are provided as a Source Data file.
