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Tumor necrosis factor-alpha (TNF-α) and TNF-related apoptosis-inducing ligand(TRAIL) are apoptosis-inducing ligands that stimulate death receptors. In thisstudy, we investigated the effects of bufotalin, a major compound in toad venom,on sensitizing TNF-α and TRAIL-induced apoptosis of HeLa cells. Bufotalin promoteddeath receptor-mediated cell death, especially TRAIL-induced apoptosis, throughactivation of caspase-3 and PARP-1. Mitochondrial Bid-dependent pathway was activatedin TNF-α-induced cell death. Cotreatment of bufotalin with TRAIL resulted in thedownregulation of anti-apoptotic proteins, including Bcl-XL, Mcl-1, survivin andXIAP, and the up-regulation of MAPKs and TRAIL receptor DR5. In addition, phosphorylationof STAT1 was strongly inhibited by bufotalin. Moreover, DR5 expression was inducedby knocking down the STAT1 expression. Moreover, the TRAIL-induced apoptotic responsewas promoted by STAT1 siRNA. Our results demonstrated that bufotalin is a powerfulsensitizer of death receptor-induced apoptosis in cancer cells.

Bufotalin sensitizes death receptor-induced apoptosis via Bid- and STAT1-dependent pathways