Fig. 6

Casticin inhibits the PI3K/mTOR/AKT pathway in BYL719-resistant cells. a, b Western blot analysis of the basal expression of PI3K110α, p-mTOR, mTOR, p-AKT, and AKT in a panel of twelve NPC cell lines. All data are presented as the mean ± standard deviation. *p < 0.05 versus NP69. c IC50 values for casticin- and BYL719-induced effects on the viability of 12 NPC cell lines after 24 h of treatment. All data are presented as the mean ± standard deviation, *p < 0.05 versus BYL719. d–f Western blot analysis of PI3K/AKT signalling in cells treated with different concentrations of casticin for 24 h. d Western blotting analysis of PI3K/AKT signalling in cells treated with different concentrations of casticin for 24 h. e, f Densitometric analysis of Western blot bands of left panel. e for S18 cells, *p < 0.05 versus 0 µM, ^#p < 0.5 versus 1 µM, ^&p < 0.5 versus 2 µM, ^‡p < 0.05 versus 4 µM; f for C666-1 *p < 0.05 versus 0 µM, ^&p < 0.5 versus 2 µM, ^‡p < 0.05 versus 4 µM. g BYL719-insensitive cells. S18 and C666-1 were treated with 4 µM casticin alone or combined with 1 µM BYL719 for 12 h. Whole cell extracts were prepared and subjected to WB analysis using antibodies against p-AKT (T 308), p-mTOR (S2448), p-mTOR(S2481) and p-S6(S240/4). All data are presented as the mean ± standard deviations. *p < 0.05 versus control