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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...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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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. |
format | Online Article Text |
id | pubmed-5779878 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
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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