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Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells
Melanoma is a common type of cutaneous tumor, but current drug treatments do not satisfy clinical practice requirements. At present, mitochondrial uncoupling is an effective antitumor treatment. Triclosan, a common antimicrobial, also acts as a mitochondrial uncoupler. The aims of the present study...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7436935/ https://www.ncbi.nlm.nih.gov/pubmed/32863906 http://dx.doi.org/10.3892/ol.2020.11934 |
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author | Jin, Jing Chen, Naiwen Pan, Huan Xie, Wenhua Xu, Hong Lei, Siyu Guo, Zhiqin Ding, Renye He, Yi Gao, Jinlai |
author_facet | Jin, Jing Chen, Naiwen Pan, Huan Xie, Wenhua Xu, Hong Lei, Siyu Guo, Zhiqin Ding, Renye He, Yi Gao, Jinlai |
author_sort | Jin, Jing |
collection | PubMed |
description | Melanoma is a common type of cutaneous tumor, but current drug treatments do not satisfy clinical practice requirements. At present, mitochondrial uncoupling is an effective antitumor treatment. Triclosan, a common antimicrobial, also acts as a mitochondrial uncoupler. The aims of the present study were to investigate the effects of triclosan on melanoma cells and the underlying mechanisms. Mitochondrial membrane potential (MMP), mitochondrial morphology, mitochondrial reactive oxygen species (mito-ROS), intracellular superoxide anion and [Ca(2+)](i) were measured using confocal microscopy. It was found that triclosan application was associated with decreased A375 cell viability in a dose- and time-dependent manner and these effects may have cell specificity. Furthermore, triclosan induced MMP depolarization, ATP content decrease, mito-ROS and [Ca(2+)](i) level increases, excessive mitochondrial fission, AMP-activated protein kinase (AMPK) activation and STAT3 inhibition. Moreover, these aforementioned effects were reversed by acetylcysteine treatment. Triclosan acute treatment also induced mitochondrial swelling, which was reversed after AMPK-knockdown associated with [Ca(2+)](i) overload. Cell death was caused by STAT3 inhibition but not AMPK activation. Moreover, triclosan induced autophagy via the ROS/AMPK/p62/microtubule-associated protein 1A/1B-light chain 3 (LC3) signaling pathway, which may serve a role in feedback protection. Collectively, the present results suggested that triclosan increased mito-ROS production in melanoma cells, following induced cell death via the STAT3/Bcl-2 pathway and autophagy via the AMPK/p62/LC3 pathway. |
format | Online Article Text |
id | pubmed-7436935 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-74369352020-08-27 Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells Jin, Jing Chen, Naiwen Pan, Huan Xie, Wenhua Xu, Hong Lei, Siyu Guo, Zhiqin Ding, Renye He, Yi Gao, Jinlai Oncol Lett Articles Melanoma is a common type of cutaneous tumor, but current drug treatments do not satisfy clinical practice requirements. At present, mitochondrial uncoupling is an effective antitumor treatment. Triclosan, a common antimicrobial, also acts as a mitochondrial uncoupler. The aims of the present study were to investigate the effects of triclosan on melanoma cells and the underlying mechanisms. Mitochondrial membrane potential (MMP), mitochondrial morphology, mitochondrial reactive oxygen species (mito-ROS), intracellular superoxide anion and [Ca(2+)](i) were measured using confocal microscopy. It was found that triclosan application was associated with decreased A375 cell viability in a dose- and time-dependent manner and these effects may have cell specificity. Furthermore, triclosan induced MMP depolarization, ATP content decrease, mito-ROS and [Ca(2+)](i) level increases, excessive mitochondrial fission, AMP-activated protein kinase (AMPK) activation and STAT3 inhibition. Moreover, these aforementioned effects were reversed by acetylcysteine treatment. Triclosan acute treatment also induced mitochondrial swelling, which was reversed after AMPK-knockdown associated with [Ca(2+)](i) overload. Cell death was caused by STAT3 inhibition but not AMPK activation. Moreover, triclosan induced autophagy via the ROS/AMPK/p62/microtubule-associated protein 1A/1B-light chain 3 (LC3) signaling pathway, which may serve a role in feedback protection. Collectively, the present results suggested that triclosan increased mito-ROS production in melanoma cells, following induced cell death via the STAT3/Bcl-2 pathway and autophagy via the AMPK/p62/LC3 pathway. D.A. Spandidos 2020-10 2020-07-30 /pmc/articles/PMC7436935/ /pubmed/32863906 http://dx.doi.org/10.3892/ol.2020.11934 Text en Copyright: © Jin et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Jin, Jing Chen, Naiwen Pan, Huan Xie, Wenhua Xu, Hong Lei, Siyu Guo, Zhiqin Ding, Renye He, Yi Gao, Jinlai Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells |
title | Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells |
title_full | Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells |
title_fullStr | Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells |
title_full_unstemmed | Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells |
title_short | Triclosan induces ROS-dependent cell death and autophagy in A375 melanoma cells |
title_sort | triclosan induces ros-dependent cell death and autophagy in a375 melanoma cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7436935/ https://www.ncbi.nlm.nih.gov/pubmed/32863906 http://dx.doi.org/10.3892/ol.2020.11934 |
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