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TIGAR, TIGAR, burning bright
Cancers cells shift their metabolism towards glycolysis in order to help them support the biosynthetic demands necessary to sustain cell proliferation and growth, adapt to stress and avoid excessive reactive oxygen species (ROS) accumulation. While the p53 tumor suppressor protein is known to inhibi...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892023/ https://www.ncbi.nlm.nih.gov/pubmed/24383451 http://dx.doi.org/10.1186/2049-3002-2-1 |
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author | Lee, Pearl Vousden, Karen H Cheung, Eric C |
author_facet | Lee, Pearl Vousden, Karen H Cheung, Eric C |
author_sort | Lee, Pearl |
collection | PubMed |
description | Cancers cells shift their metabolism towards glycolysis in order to help them support the biosynthetic demands necessary to sustain cell proliferation and growth, adapt to stress and avoid excessive reactive oxygen species (ROS) accumulation. While the p53 tumor suppressor protein is known to inhibit cell growth by inducing apoptosis, senescence and cell cycle arrest, recent studies have found that p53 is also able to influence cell metabolism. TIGAR is a p53 target that functions as a fructose-2,6-bisphosphatase, thereby lowering glycolytic flux and promoting antioxidant functions. By protecting cells from oxidative stress, TIGAR may mediate some of the tumor suppressor activity of p53 but could also contribute to tumorigenesis. Here we discuss the activities of TIGAR described so far, and the potential consequences of TIGAR expression on normal and tumor cells. |
format | Online Article Text |
id | pubmed-3892023 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-38920232014-01-15 TIGAR, TIGAR, burning bright Lee, Pearl Vousden, Karen H Cheung, Eric C Cancer Metab Review Cancers cells shift their metabolism towards glycolysis in order to help them support the biosynthetic demands necessary to sustain cell proliferation and growth, adapt to stress and avoid excessive reactive oxygen species (ROS) accumulation. While the p53 tumor suppressor protein is known to inhibit cell growth by inducing apoptosis, senescence and cell cycle arrest, recent studies have found that p53 is also able to influence cell metabolism. TIGAR is a p53 target that functions as a fructose-2,6-bisphosphatase, thereby lowering glycolytic flux and promoting antioxidant functions. By protecting cells from oxidative stress, TIGAR may mediate some of the tumor suppressor activity of p53 but could also contribute to tumorigenesis. Here we discuss the activities of TIGAR described so far, and the potential consequences of TIGAR expression on normal and tumor cells. BioMed Central 2014-01-03 /pmc/articles/PMC3892023/ /pubmed/24383451 http://dx.doi.org/10.1186/2049-3002-2-1 Text en Copyright © 2014 Lee et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. 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 Lee, Pearl Vousden, Karen H Cheung, Eric C TIGAR, TIGAR, burning bright |
title | TIGAR, TIGAR, burning bright |
title_full | TIGAR, TIGAR, burning bright |
title_fullStr | TIGAR, TIGAR, burning bright |
title_full_unstemmed | TIGAR, TIGAR, burning bright |
title_short | TIGAR, TIGAR, burning bright |
title_sort | tigar, tigar, burning bright |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3892023/ https://www.ncbi.nlm.nih.gov/pubmed/24383451 http://dx.doi.org/10.1186/2049-3002-2-1 |
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