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Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin
A main feature of cancer cells, when compared to normal ones, is a persistent pro-oxidative state that leads to an intrinsic oxidative stress. Cancer cells have higher levels of reactive oxygen species (ROS) than normal cells, and ROS are, in turn, responsible for the maintenance of the cancer pheno...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835130/ https://www.ncbi.nlm.nih.gov/pubmed/24281116 http://dx.doi.org/10.3390/cancers2021288 |
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author | Gibellini, Lara Pinti, Marcello Nasi, Milena De Biasi, Sara Roat, Erika Bertoncelli, Linda Cossarizza, Andrea |
author_facet | Gibellini, Lara Pinti, Marcello Nasi, Milena De Biasi, Sara Roat, Erika Bertoncelli, Linda Cossarizza, Andrea |
author_sort | Gibellini, Lara |
collection | PubMed |
description | A main feature of cancer cells, when compared to normal ones, is a persistent pro-oxidative state that leads to an intrinsic oxidative stress. Cancer cells have higher levels of reactive oxygen species (ROS) than normal cells, and ROS are, in turn, responsible for the maintenance of the cancer phenotype. Persistent ROS stress may induce adaptive stress responses, enabling cancer cells to survive with high levels of ROS and maintain cellular viability. However, excessive ROS levels render cancer cells highly susceptible to quercetin, one of the main dietary flavonoids. Quercetin depletes intracellular glutathione and increases intracellular ROS to a level that can cause cell death. |
format | Online Article Text |
id | pubmed-3835130 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-38351302013-11-21 Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin Gibellini, Lara Pinti, Marcello Nasi, Milena De Biasi, Sara Roat, Erika Bertoncelli, Linda Cossarizza, Andrea Cancers (Basel) Review A main feature of cancer cells, when compared to normal ones, is a persistent pro-oxidative state that leads to an intrinsic oxidative stress. Cancer cells have higher levels of reactive oxygen species (ROS) than normal cells, and ROS are, in turn, responsible for the maintenance of the cancer phenotype. Persistent ROS stress may induce adaptive stress responses, enabling cancer cells to survive with high levels of ROS and maintain cellular viability. However, excessive ROS levels render cancer cells highly susceptible to quercetin, one of the main dietary flavonoids. Quercetin depletes intracellular glutathione and increases intracellular ROS to a level that can cause cell death. MDPI 2010-06-14 /pmc/articles/PMC3835130/ /pubmed/24281116 http://dx.doi.org/10.3390/cancers2021288 Text en © 2010 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an Open Access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Review Gibellini, Lara Pinti, Marcello Nasi, Milena De Biasi, Sara Roat, Erika Bertoncelli, Linda Cossarizza, Andrea Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin |
title | Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin |
title_full | Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin |
title_fullStr | Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin |
title_full_unstemmed | Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin |
title_short | Interfering with ROS Metabolism in Cancer Cells: The Potential Role of Quercetin |
title_sort | interfering with ros metabolism in cancer cells: the potential role of quercetin |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3835130/ https://www.ncbi.nlm.nih.gov/pubmed/24281116 http://dx.doi.org/10.3390/cancers2021288 |
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