Fig. 3: GNE-493 blocks Akt-mTOR activation in prostate cancer cells.
From: GNE-493 inhibits prostate cancer cell growth via Akt-mTOR-dependent and -independent mechanisms
The priCa-1 cells were infected the recombinant adenovirus encoding the constitutively-active mutant Akt1 (caAkt1, S473D, for 72 h), followed by GNE-493 (250 nM) stimulation for designated time, control cells were treated with vehicle control; western blotting assays showed expression of listed proteins n (A); cell death (by measuring Trypan blue-positive cell percentage, B) and cell apoptosis (by measuring the TUNEL-positive nuclei percentage, C) were tested. priCa-1 cells stably expressing the lentiviral Akt1/2 shRNA (Akt1/2 shRNA, for 72 h) were stimulated with or without GNE-493 (250 nM); control shRNA lentiviral particles (“shC”) were added to the control cells. Cells were further cultivated for designated time, listed proteins were shown (D); cell death (by measuring Trypan blue-positive cell percentage, E) and apoptosis (by measuring TUNEL-positive nuclei percentage, F) were tested. The primary human prostate cancer cells, priCa-1 or priCa-2, were treated with 250 nM of GNE-493, LY294002, INK-128, or the vehicle control (0.25% DMSO, “Veh”) and cells were cultivated for 72 h, cell death (G) and cell apoptosis (H) were tested similarly. *P < 0.05 versus “Veh” group (B, C, G, and H). #P < 0.05 versus “Vec” cells (B and C). *P < 0.05 (E and F). #P < 0.05 versus GNE-493 treatment (G and H).
