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Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway

Sanggenon C is a well-known, major active agent of the flavonoid derivative of benzopyrone with valuable biological properties, including anticancer, anti-inflammatory, antimicrobial, antiviral, antithrombotic, and immune-modulatory activities. In this study, we investigated the molecular mechanisms...

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Autores principales: Chen, Li-Dong, Liu, Zhi-Hui, Zhang, Lian-Feng, Yao, Jian-Ning, Wang, Chun-Feng
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652955/
https://www.ncbi.nlm.nih.gov/pubmed/28849234
http://dx.doi.org/10.3892/or.2017.5912
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author Chen, Li-Dong
Liu, Zhi-Hui
Zhang, Lian-Feng
Yao, Jian-Ning
Wang, Chun-Feng
author_facet Chen, Li-Dong
Liu, Zhi-Hui
Zhang, Lian-Feng
Yao, Jian-Ning
Wang, Chun-Feng
author_sort Chen, Li-Dong
collection PubMed
description Sanggenon C is a well-known, major active agent of the flavonoid derivative of benzopyrone with valuable biological properties, including anticancer, anti-inflammatory, antimicrobial, antiviral, antithrombotic, and immune-modulatory activities. In this study, we investigated the molecular mechanisms by which sanggenon C mediated the induction of cell death in colorectal cancer cells (CRC). Treatment of colorectal cancer cells (LoVo, HT-29 and SW480) with sanggenon C (0, 5, 10, 20, 40 and 80 µM) resulted in inhibited proliferation of colon cancer cells. In addition, Sanggenon C (10, 20, 40 µM) induces apoptosis of HT-29 colon cancer cells as well as the increased ROS generation. Furthermore, treatment with sanggenon C increased the level of intracellular Ca(2+) and ATP, while inhibited the nitric oxide production via inhibiting inducible nitric oxide synthase expression. This resulted in the activation of mitochondrial apoptosis pathway as evidenced by the decrease in Bcl-2 protein expression. Consistently, the anti-growth and pro-apoptosis effects of sanggenon C on xenograft colon tumor were further confirmed in vivo. Collectively, our results demonstrated sanggenon C induced apoptosis of colon cancer cells by increased reactive oxygen species generation and decreased nitric oxide production, which is associated with inhibition of inducible nitric oxide synthase expression and activation of mitochondrial apoptosis pathway.
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spelling pubmed-56529552017-11-02 Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway Chen, Li-Dong Liu, Zhi-Hui Zhang, Lian-Feng Yao, Jian-Ning Wang, Chun-Feng Oncol Rep Articles Sanggenon C is a well-known, major active agent of the flavonoid derivative of benzopyrone with valuable biological properties, including anticancer, anti-inflammatory, antimicrobial, antiviral, antithrombotic, and immune-modulatory activities. In this study, we investigated the molecular mechanisms by which sanggenon C mediated the induction of cell death in colorectal cancer cells (CRC). Treatment of colorectal cancer cells (LoVo, HT-29 and SW480) with sanggenon C (0, 5, 10, 20, 40 and 80 µM) resulted in inhibited proliferation of colon cancer cells. In addition, Sanggenon C (10, 20, 40 µM) induces apoptosis of HT-29 colon cancer cells as well as the increased ROS generation. Furthermore, treatment with sanggenon C increased the level of intracellular Ca(2+) and ATP, while inhibited the nitric oxide production via inhibiting inducible nitric oxide synthase expression. This resulted in the activation of mitochondrial apoptosis pathway as evidenced by the decrease in Bcl-2 protein expression. Consistently, the anti-growth and pro-apoptosis effects of sanggenon C on xenograft colon tumor were further confirmed in vivo. Collectively, our results demonstrated sanggenon C induced apoptosis of colon cancer cells by increased reactive oxygen species generation and decreased nitric oxide production, which is associated with inhibition of inducible nitric oxide synthase expression and activation of mitochondrial apoptosis pathway. D.A. Spandidos 2017-10 2017-08-22 /pmc/articles/PMC5652955/ /pubmed/28849234 http://dx.doi.org/10.3892/or.2017.5912 Text en Copyright: © Chen 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
Chen, Li-Dong
Liu, Zhi-Hui
Zhang, Lian-Feng
Yao, Jian-Ning
Wang, Chun-Feng
Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway
title Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway
title_full Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway
title_fullStr Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway
title_full_unstemmed Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway
title_short Sanggenon C induces apoptosis of colon cancer cells via inhibition of NO production, iNOS expression and ROS activation of the mitochondrial pathway
title_sort sanggenon c induces apoptosis of colon cancer cells via inhibition of no production, inos expression and ros activation of the mitochondrial pathway
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5652955/
https://www.ncbi.nlm.nih.gov/pubmed/28849234
http://dx.doi.org/10.3892/or.2017.5912
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