Histone demethylase KDM3B protects against ferroptosis by upregulating SLC7A11.,FEBS Open Bio

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Histone demethylase KDM3B protects against ferroptosis by upregulating SLC7A11.
FEBS Open Bio ( IF 2.8 ) Pub Date : 2020-03-18 , DOI: 10.1002/2211-5463.12823
Yishu Wang ₁ , Yao Zhao ₁ , Haihua Wang ₁ , Chengliang Zhang ₂ , Meiqi Wang ₂ , Yong Yang ₁ , Xin Xu _{1,

2} , Zhenbo Hu ₁

Affiliation

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.

中文翻译：

组蛋白去甲基化酶KDM3B通过上调SLC7A11来预防肥大症。

Ferroptosis是一种由细胞代谢和铁依赖性脂质过氧化作用驱动的适应性细胞死亡。尽管已证明多种基因（包括SLC7A11和GPX4）在肥育过程中起关键作用，但对该过程的表观遗传调控知之甚少。在这里，我们报告说，KDM3B，组蛋白H3赖氨酸9脱甲基酶，可以预防由SLC7A11抑制剂Erastin引起的肥大症。HT-1080细胞中的KDM3B过表达导致组蛋白H3赖氨酸9甲基化降低。此外，KDM3B通过与转录因子ATF4协同上调SLC7A11的表达。总而言之，我们在这里将KDM3B确定为潜在的Ferroptosis表观遗传调控因子。

更新日期：2020-03-18

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