The dual role of autophagy in acute myeloid leukemia.
Acute myeloid leukemia
Apoptosis
Autophagy
Therapeutics
Journal
Journal of hematology & oncology
ISSN: 1756-8722
Titre abrégé: J Hematol Oncol
Pays: England
ID NLM: 101468937
Informations de publication
Date de publication:
07 05 2022
07 05 2022
Historique:
received:
26
10
2021
accepted:
14
04
2022
entrez:
7
5
2022
pubmed:
8
5
2022
medline:
11
5
2022
Statut:
epublish
Résumé
Acute myeloid leukemia (AML) is a severe hematologic malignancy prevalent in older patients, and the identification of potential therapeutic targets for AML is problematic. Autophagy is a lysosome-dependent catabolic pathway involved in the tumorigenesis and/or treatment of various cancers. Mounting evidence has suggested that autophagy plays a critical role in the initiation and progression of AML and anticancer responses. In this review, we describe recent updates on the multifaceted functions of autophagy linking to genetic alterations of AML. We also summarize the latest evidence for autophagy-related genes as potential prognostic predictors and drivers of AML tumorigenesis. We then discuss the crosstalk between autophagy and tumor cell metabolism into the impact on both AML progression and anti-leukemic treatment. Moreover, a series of autophagy regulators, i.e., the inhibitors and activators, are described as potential therapeutics for AML. Finally, we describe the translation of autophagy-modulating therapeutics into clinical practice. Autophagy in AML is a double-edged sword, necessitating a deeper understanding of how autophagy influences dual functions in AML tumorigenesis and anti-leukemic responses.
Identifiants
pubmed: 35526025
doi: 10.1186/s13045-022-01262-y
pii: 10.1186/s13045-022-01262-y
pmc: PMC9077970
doi:
Types de publication
Journal Article
Review
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
51Subventions
Organisme : National Research Foundation of Korea
ID : 2017R1A5A2015385
Organisme : Korea Health Industry Development Institute
ID : HR20C0025
Informations de copyright
© 2022. The Author(s).
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