Inhibition of MEK sensitizes gastric cancer cells to TRAIL-induced apoptosis

Rok, strany: 2014, 136 - 143

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), which has long been believed to be highly selective in inducing apoptosis in cancer cells, has turned out to be a molecule that induces a far more diverse range of effects. The aim of this study was to investigate whether or not ERK1/2 pathway is involved in antitumor effects of TRAIL on gastric cancer cells. In addition to activate the extrinsic and intrinsic apoptotic pathway, TRAIL also triggered the activation of ERK1/2. Inhibition of ERK1/2 signaling by MEK inhibitor U0126 promoted cell death via increased activation of caspases, drop in mitochondrial membrane potential and downregulation of XIAP, cIAP2 and Mcl-1. These results indicate that TRAIL-induced rapid activation of ERK1/2 may be a survival mechanism to struggle against TRAIL assault at the early stage, and inhibition of ERK1/2 signaling can sensitize gastric cancer cells to TRAIL-induced apoptosis. Keywords: gastric cancer, TRAIL, ERK1/2, apoptosis

ISO 690:

Wu, P., Cheng, Y., Wang, J., Zhang, X., Zhang, L. 2014. Inhibition of MEK sensitizes gastric cancer cells to TRAIL-induced apoptosis. In NEOPLASMA, vol. 61, no.2, pp. 136-143. 0028-2685.

APA:

Wu, P., Cheng, Y., Wang, J., Zhang, X., Zhang, L. (2014). Inhibition of MEK sensitizes gastric cancer cells to TRAIL-induced apoptosis. NEOPLASMA, 61(2), 136-143. 0028-2685.