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Systems biology analysis of drivers underlying hallmarks of cancer cell metabolism
Malignant transformation is often accompanied by significant metabolic changes. To identify drivers underlying these changes, we calculated metabolic flux states for the NCI60 cell line collection and correlated the variance between metabolic states of these lines with their other properties. The an...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5264163/ https://www.ncbi.nlm.nih.gov/pubmed/28120890 http://dx.doi.org/10.1038/srep41241 |
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author | Zielinski, Daniel C. Jamshidi, Neema Corbett, Austin J. Bordbar, Aarash Thomas, Alex Palsson, Bernhard O. |
author_facet | Zielinski, Daniel C. Jamshidi, Neema Corbett, Austin J. Bordbar, Aarash Thomas, Alex Palsson, Bernhard O. |
author_sort | Zielinski, Daniel C. |
collection | PubMed |
description | Malignant transformation is often accompanied by significant metabolic changes. To identify drivers underlying these changes, we calculated metabolic flux states for the NCI60 cell line collection and correlated the variance between metabolic states of these lines with their other properties. The analysis revealed a remarkably consistent structure underlying high flux metabolism. The three primary uptake pathways, glucose, glutamine and serine, are each characterized by three features: (1) metabolite uptake sufficient for the stoichiometric requirement to sustain observed growth, (2) overflow metabolism, which scales with excess nutrient uptake over the basal growth requirement, and (3) redox production, which also scales with nutrient uptake but greatly exceeds the requirement for growth. We discovered that resistance to chemotherapeutic drugs in these lines broadly correlates with the amount of glucose uptake. These results support an interpretation of the Warburg effect and glutamine addiction as features of a growth state that provides resistance to metabolic stress through excess redox and energy production. Furthermore, overflow metabolism observed may indicate that mitochondrial catabolic capacity is a key constraint setting an upper limit on the rate of cofactor production possible. These results provide a greater context within which the metabolic alterations in cancer can be understood. |
format | Online Article Text |
id | pubmed-5264163 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-52641632017-01-30 Systems biology analysis of drivers underlying hallmarks of cancer cell metabolism Zielinski, Daniel C. Jamshidi, Neema Corbett, Austin J. Bordbar, Aarash Thomas, Alex Palsson, Bernhard O. Sci Rep Article Malignant transformation is often accompanied by significant metabolic changes. To identify drivers underlying these changes, we calculated metabolic flux states for the NCI60 cell line collection and correlated the variance between metabolic states of these lines with their other properties. The analysis revealed a remarkably consistent structure underlying high flux metabolism. The three primary uptake pathways, glucose, glutamine and serine, are each characterized by three features: (1) metabolite uptake sufficient for the stoichiometric requirement to sustain observed growth, (2) overflow metabolism, which scales with excess nutrient uptake over the basal growth requirement, and (3) redox production, which also scales with nutrient uptake but greatly exceeds the requirement for growth. We discovered that resistance to chemotherapeutic drugs in these lines broadly correlates with the amount of glucose uptake. These results support an interpretation of the Warburg effect and glutamine addiction as features of a growth state that provides resistance to metabolic stress through excess redox and energy production. Furthermore, overflow metabolism observed may indicate that mitochondrial catabolic capacity is a key constraint setting an upper limit on the rate of cofactor production possible. These results provide a greater context within which the metabolic alterations in cancer can be understood. Nature Publishing Group 2017-01-25 /pmc/articles/PMC5264163/ /pubmed/28120890 http://dx.doi.org/10.1038/srep41241 Text en Copyright © 2017, The Author(s) http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Zielinski, Daniel C. Jamshidi, Neema Corbett, Austin J. Bordbar, Aarash Thomas, Alex Palsson, Bernhard O. Systems biology analysis of drivers underlying hallmarks of cancer cell metabolism |
title | Systems biology analysis of drivers underlying hallmarks of cancer cell metabolism |
title_full | Systems biology analysis of drivers underlying hallmarks of cancer cell metabolism |
title_fullStr | Systems biology analysis of drivers underlying hallmarks of cancer cell metabolism |
title_full_unstemmed | Systems biology analysis of drivers underlying hallmarks of cancer cell metabolism |
title_short | Systems biology analysis of drivers underlying hallmarks of cancer cell metabolism |
title_sort | systems biology analysis of drivers underlying hallmarks of cancer cell metabolism |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5264163/ https://www.ncbi.nlm.nih.gov/pubmed/28120890 http://dx.doi.org/10.1038/srep41241 |
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