Department of Experimental Radiation Oncology, The University of Texas MD Anderson Cancer Center, Houston, Texas.
Cancer Res. 2019 Apr 15;79(8):1749-1750. doi: 10.1158/0008-5472.CAN-19-0487.
Ferroptosis, a form of iron-dependent, nonapoptotic cell death that is induced by excessive lipid peroxidation, has been recently identified as a new tumor suppression mechanism. In this issue of , Liu and colleagues demonstrate that the deubiquitinase (DUB) OTUB1 is frequently overexpressed in human cancers, and functions to "dub" (trim) the ferroptosis process in cancer cells and promotes tumor development by stabilizing the cystine transporter, SLC7A11. This study not only reveals a hitherto unappreciated regulatory mechanism of ferroptosis but also identifies potential therapeutic targets for cancer treatment..
铁死亡是一种由脂质过氧化作用引起的铁依赖性非凋亡性细胞死亡,最近被认为是一种新的肿瘤抑制机制。在本期的《细胞》杂志中,刘博士及其同事证明去泛素化酶(DUB)OTUB1 在人类癌症中经常过表达,并通过稳定胱氨酸转运蛋白 SLC7A11 来“泛素化”(修剪)癌细胞中的铁死亡过程,从而发挥作用,促进肿瘤的发展。这项研究不仅揭示了铁死亡调控机制的一个新的未知方面,还为癌症治疗确定了潜在的治疗靶点。