Abstract
Ferroptosis is a type of adaptive cell death driven by cellular metabolism and iron‐dependent lipid peroxidation. Though multiple genes (including SLC7A11 and GPX4) have been demonstrated to play key roles in ferroptosis, little is known about the epigenetic regulation of this process. Here, we report that KDM3B, a histone H3 lysine 9 demethylase, can protect against ferroptosis induced by Erastin, an inhibitor of SLC7A11. KDM3B overexpression in HT‐1080 cells results in decreased histone H3 lysine 9 methylation. Furthermore, KDM3B upregulates the expression of SLC7A11 through cooperation with the transcription factor ATF4. In summary, we identify here KDM3B as a potential epigenetic regulator of ferroptosis.
Highlights
Yishu Wang1, Yao Zhao1, Haihua Wang1, Chengliang Zhang2, Meiqi Wang2, Yong Yang1, Xin Xu1,2 and Zhenbo Hu1
We report that KDM3B, a histone H3 lysine 9 demethylase, can protect against ferroptosis induced by Erastin, an inhibitor of SLC7A11
Though very less is known about the epigenetic regulation of ferroptosis, we have been working on histone H3 lysine 9 demethylases KDM3B in hope of elucidating its mysteries
Summary
Yishu Wang1, Yao Zhao1, Haihua Wang1, Chengliang Zhang2, Meiqi Wang2, Yong Yang1, Xin Xu1,2 and Zhenbo Hu1. Though multiple genes (including SLC7A11 and GPX4) have been demonstrated to play key roles in ferroptosis, little is known about the epigenetic regulation of this process. We report that KDM3B, a histone H3 lysine 9 demethylase, can protect against ferroptosis induced by Erastin, an inhibitor of SLC7A11. KDM3B overexpression in HT-1080 cells results in decreased histone H3 lysine 9 methylation.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
