BECN1 is a new driver of ferroptosis

Rui Kang, Shan Zhu, Herbert J. Zeh, Daniel J. Klionsky, Daolin Tang

Research output: Contribution to journalComment/debatepeer-review

120 Scopus citations


Ferroptosis is a form of regulated cell death caused by iron accumulation and oxidative injury. BECN1 is a key regulator of macroautophagy/autophagy, a catabolic process of degradation induced by starvation or other stressors. Our recent findings reveal a novel alternative mechanism by which BECN1 can promote ferroptosis through the regulation of activity of the cysteine and glutamate antiporter system xc in cancer cells. BECN1-dependent autophagy requires the formation of the BECN1-containing class III phosphatidylinositol 3-kinase (PtdIns3K) complex, whereas BECN1-dependent ferroptosis requires the formation of a BECN1-SLC7A11 complex. Furthermore, AMP-activated protein kinase (AMPK) is required for BECN1 phosphorylation to trigger formation of the BECN1-SLC7A11 complex in the process of inhibiting system xc activity and inducing lipid peroxidation. These findings suggest that the autophagy-dependent and -independent functions of BECN1 play distinct roles in regulated cell death.

Original languageEnglish (US)
Pages (from-to)2173-2175
Number of pages3
Issue number12
StatePublished - Dec 2 2018


  • AMPK
  • BECN1
  • SLC7A11
  • autophagy
  • cancer
  • chemotherapy
  • ferroptosis
  • phosphorylation
  • redox

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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