Fig. 5.

Dioscin inhibits the mTOR, PI3K and Akt and activates the ERK1/2 and JNK1/2 in human lung cancer cell lines. Cells were treated with different concentrations of dioscin (0–5 μM) for 24 h and then subjected to Western blotting with an antibody against phospho-mTOR, phospho-PI3K or phosphor-Akt (a, c). The levels of phosphorylation of ERK1/2, JNK1/2 and p38 were also investigated by Western blotting with β-actin being used as an internal control (b, d). The values under each lane indicate relative density of the band normalized to β-actin using a densitometer