TY - JOUR
T1 - Ferroptosis is a type of autophagy-dependent cell death
AU - Zhou, Borong
AU - Liu, Jiao
AU - Kang, Rui
AU - Klionsky, Daniel J.
AU - Kroemer, Guido
AU - Tang, Daolin
N1 - Funding Information:
We apologize to the researchers who were not referenced due to space limitations. We thank Dave Primm (Department of Surgery, University of Texas Southwestern Medical Center) for his critical reading of the manuscript. This work was supported by grants from the US National Institutes of Health ( R01CA160417 [D.T.], R01CA211070 [R.K.] and GM053396 [D.J.K.]), the American Cancer Society (Research Scholar Grant RSG-16-014-01-CDD [D.T.]), and the National Natural Science Foundation of China ( 81570154 [B.Z.]). GK is supported by the Ligue contre le Cancer (équipe labellisée) ; Agence National de la Recherche (ANR) – Projets blancs ; ANR under the frame of E-Rare-2, the ERA-Net for Research on Rare Diseases ; Association pour la recherche sur le cancer (ARC) ; Cancéropôle Ile-de-France ; Chancelerie des universités de Paris (Legs Poix) , Fondation pour la Recherche Médicale (FRM) ; a donation by Elior; European Research Area Network on Cardiovascular Diseases (ERA-CVD, MINOTAUR); the European Union Horizon 2020 Project Oncobiome; Fondation Carrefour; Institut National du Cancer (INCa); Inserm (HTE); Institut Universitaire de France; LeDucq Foundation; the LabEx Immuno-Oncology; the RHU Torino Lumière; the Seerave Foundation; the SIRIC Stratified Oncology Cell DNA Repair and Tumor Immune Elimination (SOCRATE);and the SIRIC Cancer Research and Personalized Medicine (CARPEM).
Publisher Copyright:
© 2019 Elsevier Ltd
PY - 2020/11
Y1 - 2020/11
N2 - 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.
AB - 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.
KW - Autophagy
KW - Cell death
KW - Ferroptosis
KW - Iron
KW - Lipid peroxidation
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U2 - 10.1016/j.semcancer.2019.03.002
DO - 10.1016/j.semcancer.2019.03.002
M3 - Review article
C2 - 30880243
AN - SCOPUS:85062947853
SN - 1044-579X
VL - 66
SP - 89
EP - 100
JO - Seminars in Cancer Biology
JF - Seminars in Cancer Biology
ER -