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NADH dehydrogenase subunit 1/4/5 promotes survival of acute myeloid leukemia by mediating specific oxidative phosphorylation

Acute myeloid leukemia (AML) is a type of hematological malignancy caused by uncontrolled clonal proliferation of hematopoietic stem cells. The special energy metabolism mode of AML relying on oxidative phosphorylation is different from the traditional ‘Warburg effect’. However, its mechanism is not...

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Autores principales: Kuang, Ye, Peng, Chuanmei, Dong, Yulin, Wang, Jia, Kong, Fanbin, Yang, Xiaoqing, Wang, Yang, Gao, Hui
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9052001/
https://www.ncbi.nlm.nih.gov/pubmed/35425997
http://dx.doi.org/10.3892/mmr.2022.12711
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author Kuang, Ye
Peng, Chuanmei
Dong, Yulin
Wang, Jia
Kong, Fanbin
Yang, Xiaoqing
Wang, Yang
Gao, Hui
author_facet Kuang, Ye
Peng, Chuanmei
Dong, Yulin
Wang, Jia
Kong, Fanbin
Yang, Xiaoqing
Wang, Yang
Gao, Hui
author_sort Kuang, Ye
collection PubMed
description Acute myeloid leukemia (AML) is a type of hematological malignancy caused by uncontrolled clonal proliferation of hematopoietic stem cells. The special energy metabolism mode of AML relying on oxidative phosphorylation is different from the traditional ‘Warburg effect’. However, its mechanism is not clear. In the present study, it was demonstrated that the mRNA expression levels of NADH dehydrogenase subunit 1, 4 and 5 (ND1, ND4 and ND5) were upregulated in AML samples from The Cancer Genome Atlas database using the limma package in the R programming language. Reverse transcription-quantitative PCR and ELISA were used to verify the upregulation of ND1, ND4 and ND5 in clinical samples. Pan-cancer analysis revealed that the expression of ND1 was upregulated only in AML, ND2 was upregulated only in AML and thymoma, and ND4 was upregulated only in AML and kidney chromophobe. In the present study, it was demonstrated that silencing of ND1/4/5 could inhibit the proliferation of AML cells in transplanted tumor of nude mice. Additionally, it was found that oxidative phosphorylation and energy metabolism of AML cells were decreased after silencing of ND1/4/5. In conclusion, the present study suggested that ND1/4/5 may be involved in the regulation of oxidative phosphorylation metabolism in AML as a potential cancer-promoting factor.
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spelling pubmed-90520012022-04-29 NADH dehydrogenase subunit 1/4/5 promotes survival of acute myeloid leukemia by mediating specific oxidative phosphorylation Kuang, Ye Peng, Chuanmei Dong, Yulin Wang, Jia Kong, Fanbin Yang, Xiaoqing Wang, Yang Gao, Hui Mol Med Rep Articles Acute myeloid leukemia (AML) is a type of hematological malignancy caused by uncontrolled clonal proliferation of hematopoietic stem cells. The special energy metabolism mode of AML relying on oxidative phosphorylation is different from the traditional ‘Warburg effect’. However, its mechanism is not clear. In the present study, it was demonstrated that the mRNA expression levels of NADH dehydrogenase subunit 1, 4 and 5 (ND1, ND4 and ND5) were upregulated in AML samples from The Cancer Genome Atlas database using the limma package in the R programming language. Reverse transcription-quantitative PCR and ELISA were used to verify the upregulation of ND1, ND4 and ND5 in clinical samples. Pan-cancer analysis revealed that the expression of ND1 was upregulated only in AML, ND2 was upregulated only in AML and thymoma, and ND4 was upregulated only in AML and kidney chromophobe. In the present study, it was demonstrated that silencing of ND1/4/5 could inhibit the proliferation of AML cells in transplanted tumor of nude mice. Additionally, it was found that oxidative phosphorylation and energy metabolism of AML cells were decreased after silencing of ND1/4/5. In conclusion, the present study suggested that ND1/4/5 may be involved in the regulation of oxidative phosphorylation metabolism in AML as a potential cancer-promoting factor. D.A. Spandidos 2022-06 2022-04-14 /pmc/articles/PMC9052001/ /pubmed/35425997 http://dx.doi.org/10.3892/mmr.2022.12711 Text en Copyright: © Kuang et al. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Kuang, Ye
Peng, Chuanmei
Dong, Yulin
Wang, Jia
Kong, Fanbin
Yang, Xiaoqing
Wang, Yang
Gao, Hui
NADH dehydrogenase subunit 1/4/5 promotes survival of acute myeloid leukemia by mediating specific oxidative phosphorylation
title NADH dehydrogenase subunit 1/4/5 promotes survival of acute myeloid leukemia by mediating specific oxidative phosphorylation
title_full NADH dehydrogenase subunit 1/4/5 promotes survival of acute myeloid leukemia by mediating specific oxidative phosphorylation
title_fullStr NADH dehydrogenase subunit 1/4/5 promotes survival of acute myeloid leukemia by mediating specific oxidative phosphorylation
title_full_unstemmed NADH dehydrogenase subunit 1/4/5 promotes survival of acute myeloid leukemia by mediating specific oxidative phosphorylation
title_short NADH dehydrogenase subunit 1/4/5 promotes survival of acute myeloid leukemia by mediating specific oxidative phosphorylation
title_sort nadh dehydrogenase subunit 1/4/5 promotes survival of acute myeloid leukemia by mediating specific oxidative phosphorylation
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9052001/
https://www.ncbi.nlm.nih.gov/pubmed/35425997
http://dx.doi.org/10.3892/mmr.2022.12711
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