Moreover, treatment with N-acetyl-L-cysteine prior to induction with TRAIL increased expression of the anti-apoptotic Bcl-2 protein. Treatment with N-acetyl-L-cysteine also inhibited expression of apoptotic proteins such as Bax and Smac and abrogated caspase-8 activation. This sensitization was inhibited by N-acetyl-l-cysteine, which restored the mitochondrial transmembrane potential and reduced reactive oxygen species generation. This effect was accompanied by reduction in mitochondrial transmembrane potential and generation of reactive oxygen species. It was found that treatment with CCCP followed by incubation with TRAIL markedly enhanced apoptosis by 2 fold compared with treatment with TRAIL alone. This study investigated the effect of carbonyl cyanide m-chlorophenylhydrazone (CCCP), a classic uncoupler of oxidative phosphorylation, on TRAIL-induced apoptosis in SNU-638 cells derived from human gastric cancer cells. TRAIL is a member of the tumor necrosis factor family and engages apoptosis via recruitment and rapid activation of caspase-8.

What is cccp in biochem