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ROS homeostasis and metabolism: a dangerous liason in cancer cells

Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage and genomic instability, and ultimately,...

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Detalles Bibliográficos
Autores principales: Panieri, E, Santoro, M M
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5143371/
https://www.ncbi.nlm.nih.gov/pubmed/27277675
http://dx.doi.org/10.1038/cddis.2016.105
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author Panieri, E
Santoro, M M
author_facet Panieri, E
Santoro, M M
author_sort Panieri, E
collection PubMed
description Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage and genomic instability, and ultimately, by reprogramming cancer cell metabolism. This review outlines the metabolic-dependent mechanisms that tumors engage in when faced with oxidative stress conditions that are critical for cancer progression by producing redox cofactors. In particular, we describe how the mitochondria has a key role in regulating the interplay between redox homeostasis and metabolism within tumor cells. Last, we will discuss the potential therapeutic use of agents that directly or indirectly block metabolism.
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spelling pubmed-51433712016-12-23 ROS homeostasis and metabolism: a dangerous liason in cancer cells Panieri, E Santoro, M M Cell Death Dis Review Tumor cells harbor genetic alterations that promote a continuous and elevated production of reactive oxygen species. Whereas such oxidative stress conditions would be harmful to normal cells, they facilitate tumor growth in multiple ways by causing DNA damage and genomic instability, and ultimately, by reprogramming cancer cell metabolism. This review outlines the metabolic-dependent mechanisms that tumors engage in when faced with oxidative stress conditions that are critical for cancer progression by producing redox cofactors. In particular, we describe how the mitochondria has a key role in regulating the interplay between redox homeostasis and metabolism within tumor cells. Last, we will discuss the potential therapeutic use of agents that directly or indirectly block metabolism. Nature Publishing Group 2016-06 2016-06-09 /pmc/articles/PMC5143371/ /pubmed/27277675 http://dx.doi.org/10.1038/cddis.2016.105 Text en Copyright © 2016 Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ Cell Death and Disease is an open-access journal published by Nature Publishing Group. 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 Review
Panieri, E
Santoro, M M
ROS homeostasis and metabolism: a dangerous liason in cancer cells
title ROS homeostasis and metabolism: a dangerous liason in cancer cells
title_full ROS homeostasis and metabolism: a dangerous liason in cancer cells
title_fullStr ROS homeostasis and metabolism: a dangerous liason in cancer cells
title_full_unstemmed ROS homeostasis and metabolism: a dangerous liason in cancer cells
title_short ROS homeostasis and metabolism: a dangerous liason in cancer cells
title_sort ros homeostasis and metabolism: a dangerous liason in cancer cells
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5143371/
https://www.ncbi.nlm.nih.gov/pubmed/27277675
http://dx.doi.org/10.1038/cddis.2016.105
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