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. 2019 Dec 15;11(12):7255–7271.

Figure 1.

Figure 1

BEZ235 significantly inhibited paclitaxel-induced activation of PI3K/Akt/mTOR pathway in HCC cells. A and B. The distribution of differential proteins on the PI3K/Akt and mTOR pathways in the paclitaxel-treated HepG2 signal map. C and C1. HepG2 cell was incubated with paclitaxel (5 μmol/L) for different time points, respectively. The cell lysates were gathered and the designated proteins (p-PI3Kp85, p-mTOR (Ser2481), p-Akt (Ser473), p-eIF4EBP1 and p-S6K1) were detected by WB, compare to the 0 h group. D and D1. HepG2 cell was incubated with various concentrations of BEZ235 for 24 h. The cell lysates were gathered and the designated proteins were detected by WB, compare to the 0 µM group. E, E1-E5. HepG2 cell was incubated under various concentrations of BEZ235 with a stable concertation of paclitaxel for 24 h. The cell lysates were gathered and the designated proteins (p-PI3Kp85, p-mTOR (Ser2481), p-Akt (Ser473), p-eIF4EBP1 and p-S6K1) were detected by WB, compared to that of the control and single drug groups. BEZ235-PTX: paclitaxel combined with BEZ235. Data expressed as mean ± SD, n=3 (*P<0.05; **P<0.01; ***P<0.001).