Fig. 6

The selective PI3K p110α inhibitor suppressed GBC progression both in the WT and E545K cells in vitro. a-d After treated with (A66) or without (CON) 15 μM/L A66 for the GBC-SD cells and 5 μM/L A66 for the NOZ cells, Cell proliferation of WT or E545K GBC-SD and NOZ cells was evaluated using CCK8 cell viability assays. Cell proliferation was represented as cell quantity. Data are presented as mean ± SD (n = 5). e-h After treated with (A66) or without (CON) 15 μM/L A66 for the GBC-SD cells and 5 μM/L A66 for the NOZ cells for 24 h, key proteins in PI3K-akt pathway were examined by Western blot assays. Representative chemiluminescent images of PI3K p110α, p-akt and akt and the relative expression quantities of p-akt (mean ± SD, n = 3) are shown. i, j PI3K p110α binding to EGFR was examined by co-immunoprecipitation assays. Representative chemiluminescent images and the relative expression quantities of PI3K p110α binding to EGFR (mean ± SD, n = 3) are shown