Ferroptosis is a type of autophagy-dependent cell death

Borong Zhou, Jiao Liu, Rui Kang, Daniel J. Klionsky, Guido Kroemer, Daolin Tang

Research output: Contribution to journalReview articlepeer-review

78 Scopus citations

Abstract

Macroautophagy (hereafter referred to as autophagy) involves an intracellular degradation and recycling system that, in a context-dependent manner, can either promote cell survival or accelerate cellular demise. Ferroptosis was originally defined in 2012 as an iron-dependent form of cancer cell death different from apoptosis, necrosis, and autophagy. However, this latter assumption came into question because, in response to ferroptosis activators (e.g., erastin and RSL3), autophagosomes accumulate, and because components of the autophagy machinery (e.g., ATG3, ATG5, ATG4B, ATG7, ATG13, and BECN1) contribute to ferroptotic cell death. In particular, NCOA4-facilitated ferritinophagy, RAB7A-dependent lipophagy, BECN1-mediated system xc inhibition, STAT3-induced lysosomal membrane permeabilization, and HSP90-associated chaperone-mediated autophagy can promote ferroptosis. In this review, we summarize current knowledge on the signaling pathways involved in ferroptosis, while focusing on the regulation of autophagy-dependent ferroptotic cell death. The molecular comprehension of these phenomena may lead to the development of novel anticancer therapies.

Original languageEnglish (US)
Pages (from-to)89-100
Number of pages12
JournalSeminars in Cancer Biology
Volume66
DOIs
StatePublished - Nov 2020

Keywords

  • Autophagy
  • Cell death
  • Ferroptosis
  • Iron
  • Lipid peroxidation

ASJC Scopus subject areas

  • Cancer Research

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