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Bufalin induced apoptosis in SCC-4 human tongue cancer cells by decreasing Bcl-2 and increasing Bax expression via the mitochondria-dependent pathway

The aim of the present study was to investigate the cytotoxic effects of bufalin on SCC-4 human tongue cancer cells. Cell morphological changes and viability were examined using phase contrast microscopy and flow cytometry, respectively. The results indicated that bufalin induced morphological chang...

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Autores principales: Chou, Han-Yu, Chueh, Fu-Shin, Ma, Yi-Shih, Wu, Rick Sai-Chuen, Liao, Ching-Lung, Chu, Yung-Lin, Fan, Ming-Jen, Huang, Wen-Wen, Chung, Jing-Gung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5779878/
https://www.ncbi.nlm.nih.gov/pubmed/28983595
http://dx.doi.org/10.3892/mmr.2017.7651
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author Chou, Han-Yu
Chueh, Fu-Shin
Ma, Yi-Shih
Wu, Rick Sai-Chuen
Liao, Ching-Lung
Chu, Yung-Lin
Fan, Ming-Jen
Huang, Wen-Wen
Chung, Jing-Gung
author_facet Chou, Han-Yu
Chueh, Fu-Shin
Ma, Yi-Shih
Wu, Rick Sai-Chuen
Liao, Ching-Lung
Chu, Yung-Lin
Fan, Ming-Jen
Huang, Wen-Wen
Chung, Jing-Gung
author_sort Chou, Han-Yu
collection PubMed
description The aim of the present study was to investigate the cytotoxic effects of bufalin on SCC-4 human tongue cancer cells. Cell morphological changes and viability were examined using phase contrast microscopy and flow cytometry, respectively. The results indicated that bufalin induced morphological changes and reduced total viable cells. Apoptotic cell death was analyzed by DAPI staining and DNA gel electrophoresis; the results revealed that bufalin induced cell apoptosis. Levels of reactive oxygen species (ROS), Ca(2+), nitric oxide (NO) and mitochondrial membrane potential (ΔΨ(m)) were measured by flow cytometry, and bufalin was observed to increase Ca(2+) and NO production, decrease the ΔΨ(m) and reduce ROS production in SCC-4 cells. In addition, western blotting was performed to detect apoptosis-associated protein expression. The results demonstrated that bufalin reduced the expression of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and increased the expression of the pro-apoptotic protein, Bcl-2-associated X protein. However, bufalin treatment also increased the expression of other apoptosis-associated proteins such as apoptosis-inducing factor and endonuclease G in SCC-4 cells. Based on these findings, bufalin may induce apoptotic cell death via mitochondria-dependent pathways in human tongue cancer SCC-4 cells.
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spelling pubmed-57798782018-02-12 Bufalin induced apoptosis in SCC-4 human tongue cancer cells by decreasing Bcl-2 and increasing Bax expression via the mitochondria-dependent pathway Chou, Han-Yu Chueh, Fu-Shin Ma, Yi-Shih Wu, Rick Sai-Chuen Liao, Ching-Lung Chu, Yung-Lin Fan, Ming-Jen Huang, Wen-Wen Chung, Jing-Gung Mol Med Rep Articles The aim of the present study was to investigate the cytotoxic effects of bufalin on SCC-4 human tongue cancer cells. Cell morphological changes and viability were examined using phase contrast microscopy and flow cytometry, respectively. The results indicated that bufalin induced morphological changes and reduced total viable cells. Apoptotic cell death was analyzed by DAPI staining and DNA gel electrophoresis; the results revealed that bufalin induced cell apoptosis. Levels of reactive oxygen species (ROS), Ca(2+), nitric oxide (NO) and mitochondrial membrane potential (ΔΨ(m)) were measured by flow cytometry, and bufalin was observed to increase Ca(2+) and NO production, decrease the ΔΨ(m) and reduce ROS production in SCC-4 cells. In addition, western blotting was performed to detect apoptosis-associated protein expression. The results demonstrated that bufalin reduced the expression of the anti-apoptotic protein B-cell lymphoma 2 (Bcl-2) and increased the expression of the pro-apoptotic protein, Bcl-2-associated X protein. However, bufalin treatment also increased the expression of other apoptosis-associated proteins such as apoptosis-inducing factor and endonuclease G in SCC-4 cells. Based on these findings, bufalin may induce apoptotic cell death via mitochondria-dependent pathways in human tongue cancer SCC-4 cells. D.A. Spandidos 2017-12 2017-09-28 /pmc/articles/PMC5779878/ /pubmed/28983595 http://dx.doi.org/10.3892/mmr.2017.7651 Text en Copyright: © Chou 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
Chou, Han-Yu
Chueh, Fu-Shin
Ma, Yi-Shih
Wu, Rick Sai-Chuen
Liao, Ching-Lung
Chu, Yung-Lin
Fan, Ming-Jen
Huang, Wen-Wen
Chung, Jing-Gung
Bufalin induced apoptosis in SCC-4 human tongue cancer cells by decreasing Bcl-2 and increasing Bax expression via the mitochondria-dependent pathway
title Bufalin induced apoptosis in SCC-4 human tongue cancer cells by decreasing Bcl-2 and increasing Bax expression via the mitochondria-dependent pathway
title_full Bufalin induced apoptosis in SCC-4 human tongue cancer cells by decreasing Bcl-2 and increasing Bax expression via the mitochondria-dependent pathway
title_fullStr Bufalin induced apoptosis in SCC-4 human tongue cancer cells by decreasing Bcl-2 and increasing Bax expression via the mitochondria-dependent pathway
title_full_unstemmed Bufalin induced apoptosis in SCC-4 human tongue cancer cells by decreasing Bcl-2 and increasing Bax expression via the mitochondria-dependent pathway
title_short Bufalin induced apoptosis in SCC-4 human tongue cancer cells by decreasing Bcl-2 and increasing Bax expression via the mitochondria-dependent pathway
title_sort bufalin induced apoptosis in scc-4 human tongue cancer cells by decreasing bcl-2 and increasing bax expression via the mitochondria-dependent pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5779878/
https://www.ncbi.nlm.nih.gov/pubmed/28983595
http://dx.doi.org/10.3892/mmr.2017.7651
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