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Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells
Solamargine, an active ingredient of Solanum nigrum, has been previously revealed to inhibit the proliferation of cancer cells. However, the effect of solamargine on human cholangiocarcinoma cells and the underlying molecular mechanism remain unknown. In the present study, the molecular mechanism un...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5920861/ https://www.ncbi.nlm.nih.gov/pubmed/29731848 http://dx.doi.org/10.3892/ol.2018.8171 |
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author | Zhang, Xiuhua Yan, Zhanpeng Xu, Tingting An, Zhentao Chen, Wanzhen Wang, Xiaosong Huang, Mengmeng Zhu, Fangshi |
author_facet | Zhang, Xiuhua Yan, Zhanpeng Xu, Tingting An, Zhentao Chen, Wanzhen Wang, Xiaosong Huang, Mengmeng Zhu, Fangshi |
author_sort | Zhang, Xiuhua |
collection | PubMed |
description | Solamargine, an active ingredient of Solanum nigrum, has been previously revealed to inhibit the proliferation of cancer cells. However, the effect of solamargine on human cholangiocarcinoma cells and the underlying molecular mechanism remain unknown. In the present study, the molecular mechanism underlying the anti-cancer effect of solamargine was assessed in human cholangiocarcinoma QBC939 cells. The results of the present study revealed that solamargine inhibited the viability of QBC939 cells in a dose-dependent manner. Furthermore, solamargine significantly induced the apoptosis of QBC939 cells and altered the mitochondrial membrane potential of cells. Quantitative polymerase chain reaction analysis revealed that solamargine decreased the mRNA level of B-cell lymphoma-2 (Bcl-2), Bcl-extra-large and X-linked inhibitor of apoptosis protein but increased the mRNA level of Bcl-2-associated X protein (Bax). In addition, western blot analysis demonstrated that solamargine inhibited the protein expression of Bcl-2 and poly ADP ribose polymerase (PARP), and promoted the protein expression of Bax, cleaved PARP, caspase 3, cleaved caspase 3 and caspase 7. Therefore, the results of the present study revealed that solamargine may induce apoptosis via the mitochondrial pathway and alter the level of apoptosis-associated proteins in human cholangiocarcinoma QBC939 cells. This in vitro study demonstrated that solamargine may be an effective chemotherapeutic agent against cholangiocarcinoma in clinical practice. |
format | Online Article Text |
id | pubmed-5920861 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-59208612018-05-04 Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells Zhang, Xiuhua Yan, Zhanpeng Xu, Tingting An, Zhentao Chen, Wanzhen Wang, Xiaosong Huang, Mengmeng Zhu, Fangshi Oncol Lett Articles Solamargine, an active ingredient of Solanum nigrum, has been previously revealed to inhibit the proliferation of cancer cells. However, the effect of solamargine on human cholangiocarcinoma cells and the underlying molecular mechanism remain unknown. In the present study, the molecular mechanism underlying the anti-cancer effect of solamargine was assessed in human cholangiocarcinoma QBC939 cells. The results of the present study revealed that solamargine inhibited the viability of QBC939 cells in a dose-dependent manner. Furthermore, solamargine significantly induced the apoptosis of QBC939 cells and altered the mitochondrial membrane potential of cells. Quantitative polymerase chain reaction analysis revealed that solamargine decreased the mRNA level of B-cell lymphoma-2 (Bcl-2), Bcl-extra-large and X-linked inhibitor of apoptosis protein but increased the mRNA level of Bcl-2-associated X protein (Bax). In addition, western blot analysis demonstrated that solamargine inhibited the protein expression of Bcl-2 and poly ADP ribose polymerase (PARP), and promoted the protein expression of Bax, cleaved PARP, caspase 3, cleaved caspase 3 and caspase 7. Therefore, the results of the present study revealed that solamargine may induce apoptosis via the mitochondrial pathway and alter the level of apoptosis-associated proteins in human cholangiocarcinoma QBC939 cells. This in vitro study demonstrated that solamargine may be an effective chemotherapeutic agent against cholangiocarcinoma in clinical practice. D.A. Spandidos 2018-05 2018-03-05 /pmc/articles/PMC5920861/ /pubmed/29731848 http://dx.doi.org/10.3892/ol.2018.8171 Text en Copyright: © Zhang 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 Zhang, Xiuhua Yan, Zhanpeng Xu, Tingting An, Zhentao Chen, Wanzhen Wang, Xiaosong Huang, Mengmeng Zhu, Fangshi Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells |
title | Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells |
title_full | Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells |
title_fullStr | Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells |
title_full_unstemmed | Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells |
title_short | Solamargine derived from Solanum nigrum induces apoptosis of human cholangiocarcinoma QBC939 cells |
title_sort | solamargine derived from solanum nigrum induces apoptosis of human cholangiocarcinoma qbc939 cells |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5920861/ https://www.ncbi.nlm.nih.gov/pubmed/29731848 http://dx.doi.org/10.3892/ol.2018.8171 |
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