Abstract：
:Ferroptosis is a newly defined form of regulated cell death characterized by the iron-dependent accumulation of lipid hydroperoxides. Erastin, the ferroptosis activator, binds to voltage-dependent anion channels VDAC2 and VDCA3, but treatment with erastin can result in the degradation of the channels. Here, the authors show that Nedd4 is induced following erastin treatment, which leads to the ubiquitination and subsequent degradation of the channels. Depletion of Nedd4 limits the protein degradation of VDAC2/3, which increases the sensitivity of cancer cells to erastin. By understanding the molecular mechanism of erastin-induced cellular resistance, we can discover how cells adapt to new molecules to maintain homeostasis. Furthermore, erastin-induced resistance mediated by FOXM1-Nedd4-VDAC2/3 negative feedback loop provides an initial framework for creating avenues to overcome the drug resistance of ferroptosis activators.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Yang Y,Luo M,Zhang K,Zhang J,Gao T,Connell DO,Yao F,Mu C,Cai B,Shang Y,Chen Wdoi
10.1038/s41467-020-14324-xsubject
Has Abstractpub_date
2020-01-23 00:00:00pages
433issue
1issn
2041-1723pii
10.1038/s41467-020-14324-xjournal_volume
11pub_type
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