Galangin and TRAIL cooperate to suppress A549 lung cancer proliferation via apoptosis and p38 MAPK activation

Abstract

Tumor necrosis factor-related apoptosis inducing ligand (TRAIL) is a promising antitumor therapy against lung cancer which is currently undergoing a phase III clinical trial in China. Unfortunately some cancer patients in the clinical trial displayed resistance to TRAIL treatment. In investigating ways to overcome this resistance, we evaluated the inhibitory effect of galangin on TRAIL resistant A549 human lung adenocarcinoma cells. Here we report that, in comparison with the single agents, the combination of galangin and TRAIL markedly suppressed proliferation of A549 cells and induced apoptosis as shown by DAPI and JC-1 staining. The combination of galangin and TRAIL induced PARP cleavage, activation of caspase-8 and p38 MAPK (mitogen-activated protein kinases). These findings indicate that the combination of galangin and TRAIL may constitute a promising strategy for the treatment of lung cancer.

Keywords

• Galangin
• TRAIL
• A549 cell line
• Cytotoxicity
• Apoptosis
• P38 MAPK