EGFR promotes ALKBH5 nuclear retention to attenuate N6-methyladenosine and protect against ferroptosis in glioblastoma
Although growth receptor pathways commonly activate similar pathways, Lv et al. show that EGF signaling represses m6A levels in contrast to induction by PDGF. EGFR blocks ALKBH5 nuclear export, increasing m6A eraser function and suppression of ferroptosis through glutathione production. ALKBH5 inhibitors enhance the anti-tumor efficacy of EGFR or glutathione inhibitors.
Source: Molecular Cell - Category: Cytology Authors: Deguan Lv, Cuiqing Zhong, Deobrat Dixit, Kailin Yang, Qiulian Wu, Bhaskar Godugu, Briana C. Prager, Guofeng Zhao, Xiuxing Wang, Qi Xie, Shideng Bao, Chuan He, Dieter Henrik Heiland, Michael G. Rosenfeld, Jeremy N. Rich Tags: Article Source Type: research