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Cancer cell lines involving cancer stem cell populations respond to oxidative stress

Cancer cells may be more prone to the accumulation of reactive oxygen species (ROS) than normal cells; therefore increased oxidative stress can specifically kill cancer cells including cancer stem cells (CSCs). In order to generate oxidative stress in various cancer cell lines including A549, G361 a...

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Detalles Bibliográficos
Autor principal: Yilmazer, Açelya
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5730381/
https://www.ncbi.nlm.nih.gov/pubmed/29276697
http://dx.doi.org/10.1016/j.btre.2017.11.004
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author Yilmazer, Açelya
author_facet Yilmazer, Açelya
author_sort Yilmazer, Açelya
collection PubMed
description Cancer cells may be more prone to the accumulation of reactive oxygen species (ROS) than normal cells; therefore increased oxidative stress can specifically kill cancer cells including cancer stem cells (CSCs). In order to generate oxidative stress in various cancer cell lines including A549, G361 and MCF-7, cultured cells were exposed to H(2)O(2). Incubation of cancer cells with H(2)O(2) results in concentration-dependent cell death in A549 and G361-7 cells, whereas MCF-7 cells showed higher sensitivity even at a lower H(2)O(2) concentration. H(2)O(2) treatment decreased the number of cells in G2/M phase and increased the number of apoptotic cells. Both CD24 negative/CD44 positive cells and CD146 positive cells were found to be present in all tested cancer cell lines, indicating that CSC populations may play role in the cellular response to oxidative stress. This study showed that inducing oxidative stress through ROS can offer a promising approach for anti-cancer therapy.
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spelling pubmed-57303812017-12-22 Cancer cell lines involving cancer stem cell populations respond to oxidative stress Yilmazer, Açelya Biotechnol Rep (Amst) Article Cancer cells may be more prone to the accumulation of reactive oxygen species (ROS) than normal cells; therefore increased oxidative stress can specifically kill cancer cells including cancer stem cells (CSCs). In order to generate oxidative stress in various cancer cell lines including A549, G361 and MCF-7, cultured cells were exposed to H(2)O(2). Incubation of cancer cells with H(2)O(2) results in concentration-dependent cell death in A549 and G361-7 cells, whereas MCF-7 cells showed higher sensitivity even at a lower H(2)O(2) concentration. H(2)O(2) treatment decreased the number of cells in G2/M phase and increased the number of apoptotic cells. Both CD24 negative/CD44 positive cells and CD146 positive cells were found to be present in all tested cancer cell lines, indicating that CSC populations may play role in the cellular response to oxidative stress. This study showed that inducing oxidative stress through ROS can offer a promising approach for anti-cancer therapy. Elsevier 2017-11-23 /pmc/articles/PMC5730381/ /pubmed/29276697 http://dx.doi.org/10.1016/j.btre.2017.11.004 Text en © 2017 Published by Elsevier B.V. http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Yilmazer, Açelya
Cancer cell lines involving cancer stem cell populations respond to oxidative stress
title Cancer cell lines involving cancer stem cell populations respond to oxidative stress
title_full Cancer cell lines involving cancer stem cell populations respond to oxidative stress
title_fullStr Cancer cell lines involving cancer stem cell populations respond to oxidative stress
title_full_unstemmed Cancer cell lines involving cancer stem cell populations respond to oxidative stress
title_short Cancer cell lines involving cancer stem cell populations respond to oxidative stress
title_sort cancer cell lines involving cancer stem cell populations respond to oxidative stress
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5730381/
https://www.ncbi.nlm.nih.gov/pubmed/29276697
http://dx.doi.org/10.1016/j.btre.2017.11.004
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