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 CoCl₂ and H₂O₂ 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 CoCl₂ and H₂O₂ 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 CoCl₂, a hypoxia-mimicking reagent, dramatically reduced the oxygen consumption rate (OCR) and increased the extracellular acidification rate (ECAR). However, H₂O₂ treatment decreased both the mitochondrial respiration and aerobic glycolysis significantly. Moreover, we found that H₂O₂ induces apoptosis in TE-1 cells through the activation of PARP, Caspase 3, and Caspase 9. Therefore, our findings indicate that CoCl₂ and H₂O₂ could cause mitochondrial dysfunction by up-regulation of ROS and regulating the cellular bioenergy metabolism, thus affecting the survival of tumor cells.