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In vivo and in vitro induction of the apoptotic effects of oxysophoridine on colorectal cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway
Oxysophoridine (OSR) is a major active alkaloid extracted from Sophoraalopecuroides L. The aim of the present study was to investigate the induction of the apoptotic effects of OSR on colorectal cancer cells in vivo and in vitro. The results of the MTT and colony formation assays demonstrated that t...
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/PMC5755128/ https://www.ncbi.nlm.nih.gov/pubmed/29344242 http://dx.doi.org/10.3892/ol.2017.7227 |
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author | Jin, Shao-Ju Yang, Yun Ma, Lei Ma, Ben-Hui Ren, Li-Ping Guo, Liu-Cheng Wang, Wen-Bao Zhang, Yan-Xin Zhao, Zhi-Jun Cui, Mingchen |
author_facet | Jin, Shao-Ju Yang, Yun Ma, Lei Ma, Ben-Hui Ren, Li-Ping Guo, Liu-Cheng Wang, Wen-Bao Zhang, Yan-Xin Zhao, Zhi-Jun Cui, Mingchen |
author_sort | Jin, Shao-Ju |
collection | PubMed |
description | Oxysophoridine (OSR) is a major active alkaloid extracted from Sophoraalopecuroides L. The aim of the present study was to investigate the induction of the apoptotic effects of OSR on colorectal cancer cells in vivo and in vitro. The results of the MTT and colony formation assays demonstrated that the proliferation of HCT116 cells was inhibited by OSR in vitro. The characteristics of cellular apoptosis in OSR-treated HCT116 cells were analyzed by Hoechst 33258 staining. It was also observed that the expression of caspase-3, B-cell lymphoma-2 (Bcl-2) associated X protein (Bax) and cytochrome c increased significantly upon OSR treatment. However, the expression of Bcl-2 and poly ADP-ribose polymerase-1 (PARP-1) was downregulated in OSR-treated cells compared with untreated cells. The in vivo experiments identified that OSR significantly inhibited the growth of the transplanted mouse CT26 tumor tissue, upregulated the expression of caspase-3, Bax and cytochrome c and downregulated the expression of Bcl-2 and PARP-1, as detected by reverse transcription-quantitative polymerase chain reaction and western blotting. It may be concluded that OSR significantly induced apoptotic effects on colorectal cancer cells in vivo and in vitro, and that its mechanism may be associated with the Bcl-2/Bax/caspase-3 signaling pathway. |
format | Online Article Text |
id | pubmed-5755128 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57551282018-01-17 In vivo and in vitro induction of the apoptotic effects of oxysophoridine on colorectal cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway Jin, Shao-Ju Yang, Yun Ma, Lei Ma, Ben-Hui Ren, Li-Ping Guo, Liu-Cheng Wang, Wen-Bao Zhang, Yan-Xin Zhao, Zhi-Jun Cui, Mingchen Oncol Lett Articles Oxysophoridine (OSR) is a major active alkaloid extracted from Sophoraalopecuroides L. The aim of the present study was to investigate the induction of the apoptotic effects of OSR on colorectal cancer cells in vivo and in vitro. The results of the MTT and colony formation assays demonstrated that the proliferation of HCT116 cells was inhibited by OSR in vitro. The characteristics of cellular apoptosis in OSR-treated HCT116 cells were analyzed by Hoechst 33258 staining. It was also observed that the expression of caspase-3, B-cell lymphoma-2 (Bcl-2) associated X protein (Bax) and cytochrome c increased significantly upon OSR treatment. However, the expression of Bcl-2 and poly ADP-ribose polymerase-1 (PARP-1) was downregulated in OSR-treated cells compared with untreated cells. The in vivo experiments identified that OSR significantly inhibited the growth of the transplanted mouse CT26 tumor tissue, upregulated the expression of caspase-3, Bax and cytochrome c and downregulated the expression of Bcl-2 and PARP-1, as detected by reverse transcription-quantitative polymerase chain reaction and western blotting. It may be concluded that OSR significantly induced apoptotic effects on colorectal cancer cells in vivo and in vitro, and that its mechanism may be associated with the Bcl-2/Bax/caspase-3 signaling pathway. D.A. Spandidos 2017-12 2017-10-19 /pmc/articles/PMC5755128/ /pubmed/29344242 http://dx.doi.org/10.3892/ol.2017.7227 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, Shao-Ju Yang, Yun Ma, Lei Ma, Ben-Hui Ren, Li-Ping Guo, Liu-Cheng Wang, Wen-Bao Zhang, Yan-Xin Zhao, Zhi-Jun Cui, Mingchen In vivo and in vitro induction of the apoptotic effects of oxysophoridine on colorectal cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway |
title | In vivo and in vitro induction of the apoptotic effects of oxysophoridine on colorectal cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway |
title_full | In vivo and in vitro induction of the apoptotic effects of oxysophoridine on colorectal cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway |
title_fullStr | In vivo and in vitro induction of the apoptotic effects of oxysophoridine on colorectal cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway |
title_full_unstemmed | In vivo and in vitro induction of the apoptotic effects of oxysophoridine on colorectal cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway |
title_short | In vivo and in vitro induction of the apoptotic effects of oxysophoridine on colorectal cancer cells via the Bcl-2/Bax/caspase-3 signaling pathway |
title_sort | in vivo and in vitro induction of the apoptotic effects of oxysophoridine on colorectal cancer cells via the bcl-2/bax/caspase-3 signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5755128/ https://www.ncbi.nlm.nih.gov/pubmed/29344242 http://dx.doi.org/10.3892/ol.2017.7227 |
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