%A Zhang,Weifen %A Gai,Chengcheng %A Ding,Dejun %A Wang,Fang %A Li,Wentong %D 2018 %J Frontiers in Oncology %C %F %G English %K ferroptosis,p53,Reactive Oxygen Species,tumor suppression,Metabolic gene,erastin %Q %R 10.3389/fonc.2018.00507 %W %L %M %P %7 %8 2018-November-02 %9 Review %# %! Targeted p53 on ferroptosis %* %< %T Targeted p53 on Small-Molecules-Induced Ferroptosis in Cancers %U https://www.frontiersin.org/articles/10.3389/fonc.2018.00507 %V 8 %0 JOURNAL ARTICLE %@ 2234-943X %X Ferroptosis is a type of programmed cell death characterized by the accumulation of lipid reactive oxygen species (L-ROS) driven by the oxidative degeneration of lipids in an iron-dependent manner. The mechanism by which lipid oxidative degradation drives ROS-ferroptosis involves metabolic dysfunctions that result in impaired intracellular metabolic processes and ROS production. Recent studies have found that p53 acts as a positive regulator of ferroptosis by promoting ROS production. p53 directly regulates the metabolic versatility of cells by favoring mitochondrial respiration, leading to ROS-mediated ferroptosis. In mild stress, p53 protects cell survival via eliminating ROS; additionally, in human colorectal cancer, p53 antagonizes ferroptosis by formation of the DPP4–p53 complex. In short, the mechanisms of p53-mediated ROS production underlying cellular response are poorly understood. In the context of recent research results, the indistinct roles of p53 on ROS-mediated ferroptosis are scrutinized to understand the mechanism underlying p53-mediated tumor suppression.