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Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum
The Traditional Chinese Medicine, Ganoderma lucidum, has been widely used for its immunity-related and anti-cancer effects. Fudan-Yueyang-Ganoderma lucidum (FYGL) is a proteoglycan, extracted from Ganoderma lucidum, that has shown safe anti-diabetic activity in vivo. The present study demonstrated t...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7693130/ https://www.ncbi.nlm.nih.gov/pubmed/33262826 http://dx.doi.org/10.3892/ol.2020.12295 |
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author | Wu, Xiao Jiang, Liping Zhang, Zeng He, Yanming Teng, Yilong Li, Jiaqi Yuan, Shilin Pan, Yanna Liang, Haohui Yang, Hongjie Zhou, Ping |
author_facet | Wu, Xiao Jiang, Liping Zhang, Zeng He, Yanming Teng, Yilong Li, Jiaqi Yuan, Shilin Pan, Yanna Liang, Haohui Yang, Hongjie Zhou, Ping |
author_sort | Wu, Xiao |
collection | PubMed |
description | The Traditional Chinese Medicine, Ganoderma lucidum, has been widely used for its immunity-related and anti-cancer effects. Fudan-Yueyang-Ganoderma lucidum (FYGL) is a proteoglycan, extracted from Ganoderma lucidum, that has shown safe anti-diabetic activity in vivo. The present study demonstrated that FYGL could selectively inhibit the viability of PANC-1 and BxPC-3 pancreatic cancer cells in a dose dependent manner, but not in Mia PaCa-2 pancreatic cancer cells and HepG2 liver cancer cells. In addition, FYGL could inhibit migration and colony formation, and promote apoptosis in PANC-1 cells, but not in Mia PaCa-2 cells. Further investigation into the underlying mechanism revealed that FYGL could inhibit the expression level of the Bcl-2 protein in PANC-1 cells, but not in Mia PaCa-2 cells, leading to an increase in reactive oxygen species (ROS) and a reduction in the mitochondrial membrane potential and cell apoptosis. The increased ROS also promoted the formation of autophagosomes, along with an increase in the microtubule-associated protein light chain 3 II/I ratio. However, FYGL halted autophagy by preventing the autophagosomes from entering the lysosomes. The inhibition of autophagy increased the accumulation of defective mitochondria, as well as the production of ROS. Taken together, the processes of ROS regulation and autophagy inhibition promoted apoptosis of PANC-1 cells through the caspase-3/cleaved caspase-3 cascade. These results indicated that FYGL could be potentially used as an anti-cancer agent in the treatment of pancreatic cancer. |
format | Online Article Text |
id | pubmed-7693130 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-76931302020-11-30 Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum Wu, Xiao Jiang, Liping Zhang, Zeng He, Yanming Teng, Yilong Li, Jiaqi Yuan, Shilin Pan, Yanna Liang, Haohui Yang, Hongjie Zhou, Ping Oncol Lett Articles The Traditional Chinese Medicine, Ganoderma lucidum, has been widely used for its immunity-related and anti-cancer effects. Fudan-Yueyang-Ganoderma lucidum (FYGL) is a proteoglycan, extracted from Ganoderma lucidum, that has shown safe anti-diabetic activity in vivo. The present study demonstrated that FYGL could selectively inhibit the viability of PANC-1 and BxPC-3 pancreatic cancer cells in a dose dependent manner, but not in Mia PaCa-2 pancreatic cancer cells and HepG2 liver cancer cells. In addition, FYGL could inhibit migration and colony formation, and promote apoptosis in PANC-1 cells, but not in Mia PaCa-2 cells. Further investigation into the underlying mechanism revealed that FYGL could inhibit the expression level of the Bcl-2 protein in PANC-1 cells, but not in Mia PaCa-2 cells, leading to an increase in reactive oxygen species (ROS) and a reduction in the mitochondrial membrane potential and cell apoptosis. The increased ROS also promoted the formation of autophagosomes, along with an increase in the microtubule-associated protein light chain 3 II/I ratio. However, FYGL halted autophagy by preventing the autophagosomes from entering the lysosomes. The inhibition of autophagy increased the accumulation of defective mitochondria, as well as the production of ROS. Taken together, the processes of ROS regulation and autophagy inhibition promoted apoptosis of PANC-1 cells through the caspase-3/cleaved caspase-3 cascade. These results indicated that FYGL could be potentially used as an anti-cancer agent in the treatment of pancreatic cancer. D.A. Spandidos 2021-01 2020-11-12 /pmc/articles/PMC7693130/ /pubmed/33262826 http://dx.doi.org/10.3892/ol.2020.12295 Text en Copyright: © Wu 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 Wu, Xiao Jiang, Liping Zhang, Zeng He, Yanming Teng, Yilong Li, Jiaqi Yuan, Shilin Pan, Yanna Liang, Haohui Yang, Hongjie Zhou, Ping Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum |
title | Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum |
title_full | Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum |
title_fullStr | Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum |
title_full_unstemmed | Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum |
title_short | Pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from Ganoderma lucidum |
title_sort | pancreatic cancer cell apoptosis is induced by a proteoglycan extracted from ganoderma lucidum |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7693130/ https://www.ncbi.nlm.nih.gov/pubmed/33262826 http://dx.doi.org/10.3892/ol.2020.12295 |
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