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Phellinus linteus activates different pathways to induce apoptosis in prostate cancer cells
It is known that polysaccharides extracted from the Phellinus linteus (PL) mushroom possess antitumour activity. We previously have demonstrated that high doses of PL render murine or human lung cancer cells susceptible to apoptosis. However, the molecular mechanisms of PL-mediated apoptosis have no...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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Nature Publishing Group
2007
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360058/ https://www.ncbi.nlm.nih.gov/pubmed/17262078 http://dx.doi.org/10.1038/sj.bjc.6603595 |
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author | Zhu, T Guo, J Collins, L Kelly, J Xiao, Z J Kim, S-H Chen, C-Y |
author_facet | Zhu, T Guo, J Collins, L Kelly, J Xiao, Z J Kim, S-H Chen, C-Y |
author_sort | Zhu, T |
collection | PubMed |
description | It is known that polysaccharides extracted from the Phellinus linteus (PL) mushroom possess antitumour activity. We previously have demonstrated that high doses of PL render murine or human lung cancer cells susceptible to apoptosis. However, the molecular mechanisms of PL-mediated apoptosis have not been fully explored. In this study, we demonstrate that LNCaP cells expressing the androgen receptor (AR) are highly susceptible to apoptosis in response to treatment with high doses of PL. In this process, caspase 8 and its downstream effectors (such as BID), as well as ER stress-related, apoptotic signalling, are activated. In contrast, a moderate amount of apoptosis occurs in PC3 cells (that lack AR) after the same treatment, which does not activate ER-mediated apoptotic signalling. We also show that, in the process of PL-induced apoptosis, caspase 2 is induced in LNCaP cells, but not in PC3 cells. However, LNCaP cells that express a mutated AR or LNCaP cells treated with a caspase 2 inhibitor blocked ER stress-induced apoptotic signals. The magnitudes of the induction of apoptosis in these cells are comparable with what occurred in the PC3 cells. The data demonstrate that high doses of PL activate the AR-dependent and independent apoptotic pathways. Our study also suggests that caspase 2 is a key target in the determination of the susceptibility of prostate cancer cells to PL-induced apoptosis. |
format | Text |
id | pubmed-2360058 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2007 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-23600582009-09-10 Phellinus linteus activates different pathways to induce apoptosis in prostate cancer cells Zhu, T Guo, J Collins, L Kelly, J Xiao, Z J Kim, S-H Chen, C-Y Br J Cancer Translational Therapeutics It is known that polysaccharides extracted from the Phellinus linteus (PL) mushroom possess antitumour activity. We previously have demonstrated that high doses of PL render murine or human lung cancer cells susceptible to apoptosis. However, the molecular mechanisms of PL-mediated apoptosis have not been fully explored. In this study, we demonstrate that LNCaP cells expressing the androgen receptor (AR) are highly susceptible to apoptosis in response to treatment with high doses of PL. In this process, caspase 8 and its downstream effectors (such as BID), as well as ER stress-related, apoptotic signalling, are activated. In contrast, a moderate amount of apoptosis occurs in PC3 cells (that lack AR) after the same treatment, which does not activate ER-mediated apoptotic signalling. We also show that, in the process of PL-induced apoptosis, caspase 2 is induced in LNCaP cells, but not in PC3 cells. However, LNCaP cells that express a mutated AR or LNCaP cells treated with a caspase 2 inhibitor blocked ER stress-induced apoptotic signals. The magnitudes of the induction of apoptosis in these cells are comparable with what occurred in the PC3 cells. The data demonstrate that high doses of PL activate the AR-dependent and independent apoptotic pathways. Our study also suggests that caspase 2 is a key target in the determination of the susceptibility of prostate cancer cells to PL-induced apoptosis. Nature Publishing Group 2007-02-26 2007-01-30 /pmc/articles/PMC2360058/ /pubmed/17262078 http://dx.doi.org/10.1038/sj.bjc.6603595 Text en Copyright © 2007 Cancer Research UK https://creativecommons.org/licenses/by/4.0/This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material.If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit https://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Translational Therapeutics Zhu, T Guo, J Collins, L Kelly, J Xiao, Z J Kim, S-H Chen, C-Y Phellinus linteus activates different pathways to induce apoptosis in prostate cancer cells |
title | Phellinus linteus activates different pathways to induce apoptosis in prostate cancer cells |
title_full | Phellinus linteus activates different pathways to induce apoptosis in prostate cancer cells |
title_fullStr | Phellinus linteus activates different pathways to induce apoptosis in prostate cancer cells |
title_full_unstemmed | Phellinus linteus activates different pathways to induce apoptosis in prostate cancer cells |
title_short | Phellinus linteus activates different pathways to induce apoptosis in prostate cancer cells |
title_sort | phellinus linteus activates different pathways to induce apoptosis in prostate cancer cells |
topic | Translational Therapeutics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2360058/ https://www.ncbi.nlm.nih.gov/pubmed/17262078 http://dx.doi.org/10.1038/sj.bjc.6603595 |
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