PRL2 serves as a negative regulator in cell adaptation to oxidative stress

作者：Xinyue Du, Yang Zhang, Xiao Li, Qi Li, Chenyun Wu, Guangjie Chen, Xiaokui Guo, Yong-qiang Weng, Zhaojun Wang · 发表于：Cell & Bioscience · 年份：2019 · DOI：10.1186/s13578-019-0358-z · 被引用次数：5 · 研究领域：Genomics, phytochemicals, and oxidative stress、Redox biology and oxidative stress、Protein Tyrosine Phosphatases

High levels of ROS cause oxidative stress, which plays a critical role in cell death. As a ROS effector protein, PRL2 senses ROS and controls phagocyte bactericidal activity during infection. Here we report PRL2 regulates oxidative stress induced cell death. PRL2 senses oxidative stress via highly reactive cysteine residues at 46 and 101. The oxidation of PRL2 causes protein degradation and supports pro-survival PDK1/AKT signal which in turn to protect cells against oxidative stress. As a result, PRL2 levels have a high correlation with oxidative stress induced cell death. In vivo experiments showed PRL2 deficient cells survive better in inflammatory oxidative environment and resist to ionizing radiation. Our finding suggests PRL2 serves as a negative regulator in cell adaptation to oxidative stress. Therefore, PRL2 could be targeted to modulate cell viability in inflammation or irradiation associated therapy.