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Mitochondria as biosynthetic factories for cancer proliferation

Unchecked growth and proliferation is a hallmark of cancer, and numerous oncogenic mutations reprogram cellular metabolism to fuel these processes. As a central metabolic organelle, mitochondria execute critical biochemical functions for the synthesis of fundamental cellular components, including fa...

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Detalles Bibliográficos
Autores principales: Ahn, Christopher S, Metallo, Christian M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4305394/
https://www.ncbi.nlm.nih.gov/pubmed/25621173
http://dx.doi.org/10.1186/s40170-015-0128-2
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author Ahn, Christopher S
Metallo, Christian M
author_facet Ahn, Christopher S
Metallo, Christian M
author_sort Ahn, Christopher S
collection PubMed
description Unchecked growth and proliferation is a hallmark of cancer, and numerous oncogenic mutations reprogram cellular metabolism to fuel these processes. As a central metabolic organelle, mitochondria execute critical biochemical functions for the synthesis of fundamental cellular components, including fatty acids, amino acids, and nucleotides. Despite the extensive interest in the glycolytic phenotype of many cancer cells, tumors contain fully functional mitochondria that support proliferation and survival. Furthermore, tumor cells commonly increase flux through one or more mitochondrial pathways, and pharmacological inhibition of mitochondrial metabolism is emerging as a potential therapeutic strategy in some cancers. Here, we review the biosynthetic roles of mitochondrial metabolism in tumors and highlight specific cancers where these processes are activated.
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spelling pubmed-43053942015-01-26 Mitochondria as biosynthetic factories for cancer proliferation Ahn, Christopher S Metallo, Christian M Cancer Metab Review Unchecked growth and proliferation is a hallmark of cancer, and numerous oncogenic mutations reprogram cellular metabolism to fuel these processes. As a central metabolic organelle, mitochondria execute critical biochemical functions for the synthesis of fundamental cellular components, including fatty acids, amino acids, and nucleotides. Despite the extensive interest in the glycolytic phenotype of many cancer cells, tumors contain fully functional mitochondria that support proliferation and survival. Furthermore, tumor cells commonly increase flux through one or more mitochondrial pathways, and pharmacological inhibition of mitochondrial metabolism is emerging as a potential therapeutic strategy in some cancers. Here, we review the biosynthetic roles of mitochondrial metabolism in tumors and highlight specific cancers where these processes are activated. BioMed Central 2015-01-25 /pmc/articles/PMC4305394/ /pubmed/25621173 http://dx.doi.org/10.1186/s40170-015-0128-2 Text en © Ahn and Metallo; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Ahn, Christopher S
Metallo, Christian M
Mitochondria as biosynthetic factories for cancer proliferation
title Mitochondria as biosynthetic factories for cancer proliferation
title_full Mitochondria as biosynthetic factories for cancer proliferation
title_fullStr Mitochondria as biosynthetic factories for cancer proliferation
title_full_unstemmed Mitochondria as biosynthetic factories for cancer proliferation
title_short Mitochondria as biosynthetic factories for cancer proliferation
title_sort mitochondria as biosynthetic factories for cancer proliferation
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4305394/
https://www.ncbi.nlm.nih.gov/pubmed/25621173
http://dx.doi.org/10.1186/s40170-015-0128-2
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