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Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia

Chemoresistance often complicates the management of cancer, as noted in the instance of acute myeloid leukemia (AML). Mitochondrial function is considered important for the viability of AML blasts and appears to also modulate chemoresistance. As mitochondrial metabolism is aberrant in AML, any disti...

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Autores principales: Feng, Lili, Zhang, Philip Y., Gao, Wenda, Yu, Jinming, Robson, Simon C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10513429/
https://www.ncbi.nlm.nih.gov/pubmed/37746249
http://dx.doi.org/10.3389/fonc.2023.1244280
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author Feng, Lili
Zhang, Philip Y.
Gao, Wenda
Yu, Jinming
Robson, Simon C.
author_facet Feng, Lili
Zhang, Philip Y.
Gao, Wenda
Yu, Jinming
Robson, Simon C.
author_sort Feng, Lili
collection PubMed
description Chemoresistance often complicates the management of cancer, as noted in the instance of acute myeloid leukemia (AML). Mitochondrial function is considered important for the viability of AML blasts and appears to also modulate chemoresistance. As mitochondrial metabolism is aberrant in AML, any distinct pathways could be directly targeted to impact both cell viability and chemoresistance. Therefore, identifying and targeting those precise rogue elements of mitochondrial metabolism could be a valid therapeutic strategy in leukemia. Here, we review the evidence for abnormalities in mitochondria metabolic processes in AML cells, that likely impact chemoresistance. We further address several therapeutic approaches targeting isocitrate dehydrogenase 2 (IDH2), CD39, nicotinamide phosphoribosyl transferase (NAMPT), electron transport chain (ETC) complex in AML and also consider the roles of mesenchymal stromal cells. We propose the term “mitotherapy” to collectively refer to such regimens that attempt to override mitochondria-mediated metabolic reprogramming, as used by cancer cells. Mounting evidence suggests that mitotherapy could provide a complementary strategy to overcome chemoresistance in liquid cancers, as well as in solid tumors.
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spelling pubmed-105134292023-09-22 Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia Feng, Lili Zhang, Philip Y. Gao, Wenda Yu, Jinming Robson, Simon C. Front Oncol Oncology Chemoresistance often complicates the management of cancer, as noted in the instance of acute myeloid leukemia (AML). Mitochondrial function is considered important for the viability of AML blasts and appears to also modulate chemoresistance. As mitochondrial metabolism is aberrant in AML, any distinct pathways could be directly targeted to impact both cell viability and chemoresistance. Therefore, identifying and targeting those precise rogue elements of mitochondrial metabolism could be a valid therapeutic strategy in leukemia. Here, we review the evidence for abnormalities in mitochondria metabolic processes in AML cells, that likely impact chemoresistance. We further address several therapeutic approaches targeting isocitrate dehydrogenase 2 (IDH2), CD39, nicotinamide phosphoribosyl transferase (NAMPT), electron transport chain (ETC) complex in AML and also consider the roles of mesenchymal stromal cells. We propose the term “mitotherapy” to collectively refer to such regimens that attempt to override mitochondria-mediated metabolic reprogramming, as used by cancer cells. Mounting evidence suggests that mitotherapy could provide a complementary strategy to overcome chemoresistance in liquid cancers, as well as in solid tumors. Frontiers Media S.A. 2023-09-07 /pmc/articles/PMC10513429/ /pubmed/37746249 http://dx.doi.org/10.3389/fonc.2023.1244280 Text en Copyright © 2023 Feng, Zhang, Gao, Yu and Robson https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Oncology
Feng, Lili
Zhang, Philip Y.
Gao, Wenda
Yu, Jinming
Robson, Simon C.
Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia
title Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia
title_full Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia
title_fullStr Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia
title_full_unstemmed Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia
title_short Targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia
title_sort targeting chemoresistance and mitochondria-dependent metabolic reprogramming in acute myeloid leukemia
topic Oncology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10513429/
https://www.ncbi.nlm.nih.gov/pubmed/37746249
http://dx.doi.org/10.3389/fonc.2023.1244280
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