Oxidative stress regulates cellular bioenergetics in esophageal squamous cell carcinoma cell

The aim of this 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 significantly reduction of 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 caused both the mitochondrial respiration and aerobic glycolysis significantly decreased. Moreover, we found that H 2 O 2 induces apoptosis of 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.