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ROS homeostasis and metabolism: a critical liaison for cancer therapy

Evidence indicates that hypoxia and oxidative stress can control metabolic reprogramming of cancer cells and other cells in tumor microenvironments and that the reprogrammed metabolic pathways in cancer tissue can also alter the redox balance. Thus, important steps toward developing novel cancer the...

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Detalles Bibliográficos
Autores principales: Kim, Jongdoo, Kim, Jaehong, Bae, Jong-Sup
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133371/
https://www.ncbi.nlm.nih.gov/pubmed/27811934
http://dx.doi.org/10.1038/emm.2016.119
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author Kim, Jongdoo
Kim, Jaehong
Bae, Jong-Sup
author_facet Kim, Jongdoo
Kim, Jaehong
Bae, Jong-Sup
author_sort Kim, Jongdoo
collection PubMed
description Evidence indicates that hypoxia and oxidative stress can control metabolic reprogramming of cancer cells and other cells in tumor microenvironments and that the reprogrammed metabolic pathways in cancer tissue can also alter the redox balance. Thus, important steps toward developing novel cancer therapy approaches would be to identify and modulate critical biochemical nodes that are deregulated in cancer metabolism and determine if the therapeutic efficiency can be influenced by changes in redox homeostasis in cancer tissues. In this review, we will explore the molecular mechanisms responsible for the metabolic reprogramming of tumor microenvironments, the functional modulation of which may disrupt the effects of or may be disrupted by redox homeostasis modulating cancer therapy.
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spelling pubmed-51333712016-12-16 ROS homeostasis and metabolism: a critical liaison for cancer therapy Kim, Jongdoo Kim, Jaehong Bae, Jong-Sup Exp Mol Med Review Evidence indicates that hypoxia and oxidative stress can control metabolic reprogramming of cancer cells and other cells in tumor microenvironments and that the reprogrammed metabolic pathways in cancer tissue can also alter the redox balance. Thus, important steps toward developing novel cancer therapy approaches would be to identify and modulate critical biochemical nodes that are deregulated in cancer metabolism and determine if the therapeutic efficiency can be influenced by changes in redox homeostasis in cancer tissues. In this review, we will explore the molecular mechanisms responsible for the metabolic reprogramming of tumor microenvironments, the functional modulation of which may disrupt the effects of or may be disrupted by redox homeostasis modulating cancer therapy. Nature Publishing Group 2016-11 2016-11-04 /pmc/articles/PMC5133371/ /pubmed/27811934 http://dx.doi.org/10.1038/emm.2016.119 Text en Copyright © 2016 The Author(s) http://creativecommons.org/licenses/by-nc-sa/4.0/ This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 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-nc-sa/4.0/
spellingShingle Review
Kim, Jongdoo
Kim, Jaehong
Bae, Jong-Sup
ROS homeostasis and metabolism: a critical liaison for cancer therapy
title ROS homeostasis and metabolism: a critical liaison for cancer therapy
title_full ROS homeostasis and metabolism: a critical liaison for cancer therapy
title_fullStr ROS homeostasis and metabolism: a critical liaison for cancer therapy
title_full_unstemmed ROS homeostasis and metabolism: a critical liaison for cancer therapy
title_short ROS homeostasis and metabolism: a critical liaison for cancer therapy
title_sort ros homeostasis and metabolism: a critical liaison for cancer therapy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5133371/
https://www.ncbi.nlm.nih.gov/pubmed/27811934
http://dx.doi.org/10.1038/emm.2016.119
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