PMID- 34207482
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20210705
IS  - 2079-7737 (Print)
IS  - 2079-7737 (Electronic)
IS  - 2079-7737 (Linking)
VI  - 10
IP  - 6
DP  - 2021 Jun 18
TI  - Autophagy a Close Relative of AML Biology.
LID - 10.3390/biology10060552 [doi]
LID - 552
AB  - Autophagy, which literally means "eat yourself", is more than just a lysosomal 
      degradation pathway. It is a well-known regulator of cellular metabolism and a 
      mechanism implicated in tumor initiation/progression and therapeutic resistance 
      in many cancers. However, whether autophagy acts as a tumor suppressor or 
      promoter is still a matter of debate. In acute myeloid leukemia (AML), it is now 
      proven that autophagy supports cell proliferation in vitro and leukemic 
      progression in vivo. Mitophagy, the specific degradation of mitochondria through 
      autophagy, was recently shown to be required for leukemic stem cell functions and 
      survival, highlighting the prominent role of this selective autophagy in leukemia 
      initiation and progression. Moreover, autophagy in AML sustains fatty acid 
      oxidation through lipophagy to support mitochondrial oxidative phosphorylation 
      (OxPHOS), a hallmark of chemotherapy-resistant cells. Nevertheless, in the 
      context of therapy, in AML, as well as in other cancers, autophagy could be 
      either cytoprotective or cytotoxic, depending on the drugs used. This review 
      summarizes the recent findings that mechanistically show how autophagy favors 
      leukemic transformation of normal hematopoietic stem cells, as well as AML 
      progression and also recapitulates its ambivalent role in resistance to 
      chemotherapies and targeted therapies.
FAU - Joffre, Carine
AU  - Joffre C
AUID- ORCID: 0000-0002-7551-356X
AD  - Centre de Recherches en Cancerologie de Toulouse (CRCT), Universite de Toulouse, 
      Inserm, CNRS, 31037 Toulouse, France.
FAU - Ducau, Charlotte
AU  - Ducau C
AD  - Centre de Recherches en Cancerologie de Toulouse (CRCT), Universite de Toulouse, 
      Inserm, CNRS, 31037 Toulouse, France.
FAU - Poillet-Perez, Laura
AU  - Poillet-Perez L
AD  - Centre de Recherches en Cancerologie de Toulouse (CRCT), Universite de Toulouse, 
      Inserm, CNRS, 31037 Toulouse, France.
FAU - Courdy, Charly
AU  - Courdy C
AD  - Centre de Recherches en Cancerologie de Toulouse (CRCT), Universite de Toulouse, 
      Inserm, CNRS, 31037 Toulouse, France.
FAU - Mansat-De Mas, Veronique
AU  - Mansat-De Mas V
AUID- ORCID: 0000-0003-1878-9129
AD  - Centre de Recherches en Cancerologie de Toulouse (CRCT), Universite de Toulouse, 
      Inserm, CNRS, 31037 Toulouse, France.
AD  - Centre Hospitalo-Universitaire (CHU) de Toulouse, Institut Universitaire du 
      Cancer de Toulouse-Oncopole (IUCT-O), 31059 Toulouse, France.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20210618
PL  - Switzerland
TA  - Biology (Basel)
JT  - Biology
JID - 101587988
PMC - PMC8235674
OTO - NOTNLM
OT  - AML
OT  - autophagy
OT  - hematopoiesis
OT  - mitophagy
OT  - therapy
COIS- The authors declare no conflict of interest.
EDAT- 2021/07/03 06:00
MHDA- 2021/07/03 06:01
PMCR- 2021/06/18
CRDT- 2021/07/02 01:31
PHST- 2021/05/11 00:00 [received]
PHST- 2021/06/10 00:00 [revised]
PHST- 2021/06/18 00:00 [accepted]
PHST- 2021/07/02 01:31 [entrez]
PHST- 2021/07/03 06:00 [pubmed]
PHST- 2021/07/03 06:01 [medline]
PHST- 2021/06/18 00:00 [pmc-release]
AID - biology10060552 [pii]
AID - biology-10-00552 [pii]
AID - 10.3390/biology10060552 [doi]
PST - epublish
SO  - Biology (Basel). 2021 Jun 18;10(6):552. doi: 10.3390/biology10060552.