Oxidative stress regulates cellular bioenergetics in esophageal squamous cell carcinoma cell

The aim of the present study was to explore the effects of oxidative stress induced by CoCl(2) and H(2)O(2) on the regulation of bioenergetics of esophageal squamous cell carcinoma (ESCC) cell line TE-1 and analyze its underlying mechanism. Western blot results showed that CoCl(2) and H(2)O(2) treatment of TE-1 cells led to significant reduction in mitochondrial respiratory chain complex subunits expression and increasing intracellular reactive oxygen species (ROS) production. We further found that TE-1 cells treated with CoCl(2), a hypoxia-mimicking reagent, dramatically reduced the oxygen consumption rate (OCR) and increased the extracellular acidification rate (ECAR). However, H(2)O(2) treatment decreased both the mitochondrial respiration and aerobic glycolysis significantly. Moreover, we found that H(2)O(2) induces apoptosis in TE-1 cells through the activation of PARP, Caspase 3, and Caspase 9. Therefore, our findings indicate that CoCl(2) and H(2)O(2) could cause mitochondrial dysfunction by up-regulation of ROS and regulating the cellular bioenergy metabolism, thus affecting the survival of tumor cells.