Investigating the effects of acute oxidative stress on the expression, localization and activity of cell death regulatory protein BNIP3
BNIP3 is a BCL2 family member that promotes cell death or survival depending on expression level and localization. During hypoxia BNIP3 levels increase and localize to mitochondria, inducing autophagic cell death. Although hypoxic regions are common in solid tumors, BNIP3 expression in these cells promotes cell survival and more aggressive disease. ROS may play a role in regulating cellular response to hypoxia and is known to induce autophagy. However, BNIP3’s role in regulating oxidative stress-induced cell death is unknown and the focus of this study. Effects of hydrogen peroxide exposure on expression, localization and function of BNIP3 were explored using HEK293, U87 and MEF cells. BNIP3 expression and colocalization with mitochondria increased after treatment, along with cell death. However, knockdown of BNIP3 provided minor protection, suggesting that BNIP3 is not required for cell death induced by acute oxidative stress. Overall, BNIP3 may regulate oxidative stress-induced cell death in some cells.