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The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines
It has been shown previously that molecules built on benzanilide and thiobenzanilide scaffolds possess differential biological properties including selective anticancer activity. In our previous study, we examined the cytotoxic activity and mechanism of action of the thiobenzanilide derivative N,N′-...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6736908/ https://www.ncbi.nlm.nih.gov/pubmed/30498945 http://dx.doi.org/10.1007/s10637-018-0704-8 |
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author | Kucinska, Malgorzata Mieszczak, Helena Piotrowska-Kempisty, Hanna Kaczmarek, Mariusz Granig, Walter Murias, Marek Erker, Thomas |
author_facet | Kucinska, Malgorzata Mieszczak, Helena Piotrowska-Kempisty, Hanna Kaczmarek, Mariusz Granig, Walter Murias, Marek Erker, Thomas |
author_sort | Kucinska, Malgorzata |
collection | PubMed |
description | It has been shown previously that molecules built on benzanilide and thiobenzanilide scaffolds possess differential biological properties including selective anticancer activity. In our previous study, we examined the cytotoxic activity and mechanism of action of the thiobenzanilide derivative N,N′-(1,2-phenylene)bis3,4,5–trifluorobenzothioamide (63 T) as a potential chemotherapeutic compound in an experimental model employing A549 lung adenocarcinoma cells and CCD39Lu non-tumorigenic lung fibroblasts. Since the results suggested oxidative stress as a co-existing mechanism of the cytotoxic effect exerted by 63 T on tested cells, studies involving the analysis of reactive oxygen species (ROS) generation and markers of oxidative stress in cells incubated with 63 T were carried out. It may be concluded that the selective activity of 63 T against cancer cells shown in our experiments is caused, at least in part, by the response of the tested cells to 63 T mediated oxidative stress in both tested cell lines. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s10637-018-0704-8) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-6736908 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-67369082019-09-23 The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines Kucinska, Malgorzata Mieszczak, Helena Piotrowska-Kempisty, Hanna Kaczmarek, Mariusz Granig, Walter Murias, Marek Erker, Thomas Invest New Drugs Preclinical Studies It has been shown previously that molecules built on benzanilide and thiobenzanilide scaffolds possess differential biological properties including selective anticancer activity. In our previous study, we examined the cytotoxic activity and mechanism of action of the thiobenzanilide derivative N,N′-(1,2-phenylene)bis3,4,5–trifluorobenzothioamide (63 T) as a potential chemotherapeutic compound in an experimental model employing A549 lung adenocarcinoma cells and CCD39Lu non-tumorigenic lung fibroblasts. Since the results suggested oxidative stress as a co-existing mechanism of the cytotoxic effect exerted by 63 T on tested cells, studies involving the analysis of reactive oxygen species (ROS) generation and markers of oxidative stress in cells incubated with 63 T were carried out. It may be concluded that the selective activity of 63 T against cancer cells shown in our experiments is caused, at least in part, by the response of the tested cells to 63 T mediated oxidative stress in both tested cell lines. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s10637-018-0704-8) contains supplementary material, which is available to authorized users. Springer US 2018-11-29 2019 /pmc/articles/PMC6736908/ /pubmed/30498945 http://dx.doi.org/10.1007/s10637-018-0704-8 Text en © The Author(s) 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. |
spellingShingle | Preclinical Studies Kucinska, Malgorzata Mieszczak, Helena Piotrowska-Kempisty, Hanna Kaczmarek, Mariusz Granig, Walter Murias, Marek Erker, Thomas The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines |
title | The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines |
title_full | The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines |
title_fullStr | The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines |
title_full_unstemmed | The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines |
title_short | The role of oxidative stress in 63 T-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines |
title_sort | role of oxidative stress in 63 t-induced cytotoxicity against human lung cancer and normal lung fibroblast cell lines |
topic | Preclinical Studies |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6736908/ https://www.ncbi.nlm.nih.gov/pubmed/30498945 http://dx.doi.org/10.1007/s10637-018-0704-8 |
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