Proteasome inhibitor bortezomi-induced the apoptosis of laryngeal squamous cell carcinoma Hep-2 cell line via disrupting redox equilibrium.

Bortezomib, a proteasome inhibitor, has been therapeutic effects in some solid tumors. In the present work, the effects of bortezomib on laryngeal squamous cell carcinoma Hep-2 cell line was investigated and the role of redox equilibrium was explored. The results showed that bortezomib decreased the cell viability and increased the apoptosis in Hep-2 cells. In addition, bortezomib overproduced reactive oxygen species (ROS) and induced the loss of mitochondrial membrane potential (ΔΨ(m)). And the activity of caspase-3 increased. N-acetyl-L-cysteine (L-NAC), a ROS scavenger, alleviated oxidative stress and inhibited the apoptosis induced by bortezomib. However, buthionine sulfoximine (BSO), an inhibitor of GSH synthetase, aggravated bortezomib-induced oxidative stress and apoptosis. So bortezomi-induced the apoptosis of Hep-2 cells via disrupting redox equilibrium.