Arsenic trioxide-induced neuroblastoma cell death is accompanied by proteolytic activation of nuclear Bax.
Arsenic trioxide (As2O3) is toxic to multidrug-resistant neuroblastoma cells in vivo and in vitro. In neuroblastoma, As2O3 does not exert its cell death-promoting effects via a classical apoptotic pathway. A death mechanism involving proteolytic cleavage of Bax to a p18 form seems to be of importance, because inhibition of Bax cleavage coincides with diminished cell death. As existing models of ce
