Autophagy a Close Relative of AML Biology
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 su...
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doaj-802362d4442f43d5a8ba9742cda3f1d62021-07-01T00:35:54ZengMDPI AGBiology2079-77372021-06-011055255210.3390/biology10060552Autophagy a Close Relative of AML BiologyCarine Joffre0Charlotte Ducau1Laura Poillet-Perez2Charly Courdy3Véronique Mansat-De Mas4Centre de Recherches en Cancérologie de Toulouse (CRCT), Université de Toulouse, Inserm, CNRS, 31037 Toulouse, FranceCentre de Recherches en Cancérologie de Toulouse (CRCT), Université de Toulouse, Inserm, CNRS, 31037 Toulouse, FranceCentre de Recherches en Cancérologie de Toulouse (CRCT), Université de Toulouse, Inserm, CNRS, 31037 Toulouse, FranceCentre de Recherches en Cancérologie de Toulouse (CRCT), Université de Toulouse, Inserm, CNRS, 31037 Toulouse, FranceCentre de Recherches en Cancérologie de Toulouse (CRCT), Université de Toulouse, Inserm, CNRS, 31037 Toulouse, FranceAutophagy, 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.https://www.mdpi.com/2079-7737/10/6/552autophagymitophagyhematopoiesisAMLtherapy |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Carine Joffre Charlotte Ducau Laura Poillet-Perez Charly Courdy Véronique Mansat-De Mas |
spellingShingle |
Carine Joffre Charlotte Ducau Laura Poillet-Perez Charly Courdy Véronique Mansat-De Mas Autophagy a Close Relative of AML Biology Biology autophagy mitophagy hematopoiesis AML therapy |
author_facet |
Carine Joffre Charlotte Ducau Laura Poillet-Perez Charly Courdy Véronique Mansat-De Mas |
author_sort |
Carine Joffre |
title |
Autophagy a Close Relative of AML Biology |
title_short |
Autophagy a Close Relative of AML Biology |
title_full |
Autophagy a Close Relative of AML Biology |
title_fullStr |
Autophagy a Close Relative of AML Biology |
title_full_unstemmed |
Autophagy a Close Relative of AML Biology |
title_sort |
autophagy a close relative of aml biology |
publisher |
MDPI AG |
series |
Biology |
issn |
2079-7737 |
publishDate |
2021-06-01 |
description |
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. |
topic |
autophagy mitophagy hematopoiesis AML therapy |
url |
https://www.mdpi.com/2079-7737/10/6/552 |
work_keys_str_mv |
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