p53-Induced ROS-accumulation induces programmed cell death in C6 glioma cells

摘要

Background and purpose: As one of the major types of programmed cell death (PCD), necrosis has been observed and demonstrated to be responsible for cell death and the mechanisms responsible for necrosis are still not very clear. This study reviews that programmed cell death (PCD), including apoptosis and necrosis for C6 glioma cells is related to p53-reactive oxygen species (ROS). Methods: The C6 glioma cells were treated with N-acetylcysteine (NAC) and assayed for cell survival, cellular ROS levels by flow cytometry assays, and western blot assay for p53 expression. C6 glioma cells were compared to downregulation of ROS levels and p53 expression, respectively pretreated with p-fifty three inhibitor-alpha (PFT-a) and N-acetylcysteine (NAC). Results: C6 glioma cells showed a significant decrease (∼2-fold) in DHE-fluorescence after NAC treatment. Interestingly, the accumulation of ROS was elevated with p53 expression in C6 glioma cells. The increase in ROS levels was followed by a decrease in cell growth and viability, and increase in the percentage of cells with necrosis. Conclusions: p53 overexpression enhanced p53-induced ROS-accumulation, which was accompanied by an increase in cell death with necrosis. These results support the hypothesis that there is a close relationship between regulating p53-induced ROS-accumulation and apoptosis and necrosis in C6 glioma cells.