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Lomefloxacin Induces Oxidative Stress and Apoptosis in COLO829 Melanoma Cells
Although some fluoroquinolones have been found to exert anti-tumor activity, studies on the effect of these drugs on melanoma cells are relatively rare. The aim of this study was to examine the effect of lomefloxacin on cell viability, reactive oxygen species production, redox balance, cell cycle di...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5666875/ https://www.ncbi.nlm.nih.gov/pubmed/29053584 http://dx.doi.org/10.3390/ijms18102194 |
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author | Beberok, Artur Wrześniok, Dorota Szlachta, Martyna Rok, Jakub Rzepka, Zuzanna Respondek, Michalina Buszman, Ewa |
author_facet | Beberok, Artur Wrześniok, Dorota Szlachta, Martyna Rok, Jakub Rzepka, Zuzanna Respondek, Michalina Buszman, Ewa |
author_sort | Beberok, Artur |
collection | PubMed |
description | Although some fluoroquinolones have been found to exert anti-tumor activity, studies on the effect of these drugs on melanoma cells are relatively rare. The aim of this study was to examine the effect of lomefloxacin on cell viability, reactive oxygen species production, redox balance, cell cycle distribution, DNA fragmentation, and apoptosis in COLO829 melanoma cells. Lomefloxacin decreases the cell viability in a dose- and time-dependent manner. For COLO829 cells treated with the drug for 24, 48, and 72 h, the values of IC50 were found to be 0.51, 0.33, and 0.25 mmol/L, respectively. The analyzed drug also altered the redox signaling pathways, as shown by intracellular reactive oxygen species overproduction and endogeneous glutathione depletion. After lomefloxacin treatment, the cells were arrested in S- and G2/M-phase, suggesting a mechanism related to topoisomerase II inhibition. DNA fragmentation was observed when the cells were exposed to increasing lomefloxacin concentrations and a prolongation of incubation time. Moreover, it was demonstrated that the drug induced mitochondrial membrane breakdown as an early hallmark of apoptosis. The obtained results provide a strong molecular basis for the pharmacologic effect underlying the potential use of lomefloxacin as a valuable agent for the treatment of melanoma in vivo. |
format | Online Article Text |
id | pubmed-5666875 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-56668752017-11-09 Lomefloxacin Induces Oxidative Stress and Apoptosis in COLO829 Melanoma Cells Beberok, Artur Wrześniok, Dorota Szlachta, Martyna Rok, Jakub Rzepka, Zuzanna Respondek, Michalina Buszman, Ewa Int J Mol Sci Article Although some fluoroquinolones have been found to exert anti-tumor activity, studies on the effect of these drugs on melanoma cells are relatively rare. The aim of this study was to examine the effect of lomefloxacin on cell viability, reactive oxygen species production, redox balance, cell cycle distribution, DNA fragmentation, and apoptosis in COLO829 melanoma cells. Lomefloxacin decreases the cell viability in a dose- and time-dependent manner. For COLO829 cells treated with the drug for 24, 48, and 72 h, the values of IC50 were found to be 0.51, 0.33, and 0.25 mmol/L, respectively. The analyzed drug also altered the redox signaling pathways, as shown by intracellular reactive oxygen species overproduction and endogeneous glutathione depletion. After lomefloxacin treatment, the cells were arrested in S- and G2/M-phase, suggesting a mechanism related to topoisomerase II inhibition. DNA fragmentation was observed when the cells were exposed to increasing lomefloxacin concentrations and a prolongation of incubation time. Moreover, it was demonstrated that the drug induced mitochondrial membrane breakdown as an early hallmark of apoptosis. The obtained results provide a strong molecular basis for the pharmacologic effect underlying the potential use of lomefloxacin as a valuable agent for the treatment of melanoma in vivo. MDPI 2017-10-20 /pmc/articles/PMC5666875/ /pubmed/29053584 http://dx.doi.org/10.3390/ijms18102194 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Beberok, Artur Wrześniok, Dorota Szlachta, Martyna Rok, Jakub Rzepka, Zuzanna Respondek, Michalina Buszman, Ewa Lomefloxacin Induces Oxidative Stress and Apoptosis in COLO829 Melanoma Cells |
title | Lomefloxacin Induces Oxidative Stress and Apoptosis in COLO829 Melanoma Cells |
title_full | Lomefloxacin Induces Oxidative Stress and Apoptosis in COLO829 Melanoma Cells |
title_fullStr | Lomefloxacin Induces Oxidative Stress and Apoptosis in COLO829 Melanoma Cells |
title_full_unstemmed | Lomefloxacin Induces Oxidative Stress and Apoptosis in COLO829 Melanoma Cells |
title_short | Lomefloxacin Induces Oxidative Stress and Apoptosis in COLO829 Melanoma Cells |
title_sort | lomefloxacin induces oxidative stress and apoptosis in colo829 melanoma cells |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5666875/ https://www.ncbi.nlm.nih.gov/pubmed/29053584 http://dx.doi.org/10.3390/ijms18102194 |
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