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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...

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Detalles Bibliográficos
Autores principales: Lee, Pearl, Vousden, Karen H, Cheung, Eric C
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2014
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.
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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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