TRAIL-induced apoptosis enhanced by paclitaxel in gastric cancer BGC823 cells

Objective To observe the inhibition effect of paclitaxel on tumor necrosis factor-related apoptosis-inducing ligand(TRAIL)-induced apoptosis in gastric cancer BGC823 cells.Methods Gastric cancer BGC823 cells were routinely subcultured,and the used cells were all from the logarithmic growth phase.Cell proliferation was measured using MTT assay.Cell apoptosis was determined by flow cytometry.The expressions of Akt and phosphor-Akt were determined by Western blotting.Results Treatment with 100 ng/mL TRAIL resulted in a little cell apoptosis in BGC823 cells.Meanwhile,the phosphorylation of Akt was detected.Treatment with paclitaxel for 24 hours,the IC50 dose was 8.97 μg/ml.Compared to treatment with TRAIL or paclitaxel alone,treatment with TRAIL(100 ng/ml) and paclitaxel(8.97 μg/ml,IC50 dose of 24 h) leaded to a dramatic increase in cell apoptosis(P0.05).Western blotting showed that TRAIL(100 ng/ml) alone induced the activation of Akt for 24 hours in BGC823 cells.While 8.97 μg/ml paclitaxel significantly inhibited the phosphorylation of Akt.Treatment with TRAIL(100 ng/ml)and paclitaxel(8.97 μg/ml) also prevented the phosphorylation of Akt induced by TRAIL.Conclusion Paclitaxel enhance TRAIL-induced apoptosis in gastric cancer BGC823 cells by the inhibition of Akt phosphorylation induced by TRAIL.