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Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling
BACKGROUND: Although the incidence of pancreatic cancer has increased markedly, the 5-year survival rate for this disease is considerably low compared with other types of cancer. Moreover, the mortality rate of pancreatic cancer is similar to its incidence rate. Current therapeutic agents exhibit a...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2019
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927568/ https://www.ncbi.nlm.nih.gov/pubmed/31908533 http://dx.doi.org/10.2147/CMAR.S228926 |
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author | Ni, Fubiao Tang, Hengjie Wang, Cheng Zhang, Hewei Zheng, Chenlei Zhang, Ning Chen, Bicheng Sun, Linxiao |
author_facet | Ni, Fubiao Tang, Hengjie Wang, Cheng Zhang, Hewei Zheng, Chenlei Zhang, Ning Chen, Bicheng Sun, Linxiao |
author_sort | Ni, Fubiao |
collection | PubMed |
description | BACKGROUND: Although the incidence of pancreatic cancer has increased markedly, the 5-year survival rate for this disease is considerably low compared with other types of cancer. Moreover, the mortality rate of pancreatic cancer is similar to its incidence rate. Current therapeutic agents exhibit a lack of specificity for pancreatic cancer. Baohuoside I is traditionally used to treat orgasmic disorder and inflammation. However, its role in pancreatic cancer is unknown. OBJECTIVE: To explore the effects of Baohuoside I on pancreatic cancer and to study the potential-related molecular mechanism. MATERIALS AND METHODS: In the present study, the antineoplastic effect of Baohuoside I was investigated with regard to pancreatic cancer via colony formation, transwell and migration assay. The energy metabolism changes of pancreatic cancer were tested by flow cytometry analysis and oxidative phosphorylation and glycolysis assay. The target signaling members were analyzed by Western blot. RESULTS: Baohuoside I inhibited the cell growth of pancreatic cancer cells. In addition, it affected intracellular energy metabolism to induce cancer cell apoptosis via the mTOR/S6K1 and the caspase/Bcl2/Bax signaling pathways. CONCLUSION: The present data provide further insight into the development of novel drugs against pancreatic cancer. |
format | Online Article Text |
id | pubmed-6927568 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-69275682020-01-06 Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling Ni, Fubiao Tang, Hengjie Wang, Cheng Zhang, Hewei Zheng, Chenlei Zhang, Ning Chen, Bicheng Sun, Linxiao Cancer Manag Res Original Research BACKGROUND: Although the incidence of pancreatic cancer has increased markedly, the 5-year survival rate for this disease is considerably low compared with other types of cancer. Moreover, the mortality rate of pancreatic cancer is similar to its incidence rate. Current therapeutic agents exhibit a lack of specificity for pancreatic cancer. Baohuoside I is traditionally used to treat orgasmic disorder and inflammation. However, its role in pancreatic cancer is unknown. OBJECTIVE: To explore the effects of Baohuoside I on pancreatic cancer and to study the potential-related molecular mechanism. MATERIALS AND METHODS: In the present study, the antineoplastic effect of Baohuoside I was investigated with regard to pancreatic cancer via colony formation, transwell and migration assay. The energy metabolism changes of pancreatic cancer were tested by flow cytometry analysis and oxidative phosphorylation and glycolysis assay. The target signaling members were analyzed by Western blot. RESULTS: Baohuoside I inhibited the cell growth of pancreatic cancer cells. In addition, it affected intracellular energy metabolism to induce cancer cell apoptosis via the mTOR/S6K1 and the caspase/Bcl2/Bax signaling pathways. CONCLUSION: The present data provide further insight into the development of novel drugs against pancreatic cancer. Dove 2019-12-19 /pmc/articles/PMC6927568/ /pubmed/31908533 http://dx.doi.org/10.2147/CMAR.S228926 Text en © 2019 Ni et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Ni, Fubiao Tang, Hengjie Wang, Cheng Zhang, Hewei Zheng, Chenlei Zhang, Ning Chen, Bicheng Sun, Linxiao Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling |
title | Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling |
title_full | Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling |
title_fullStr | Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling |
title_full_unstemmed | Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling |
title_short | Baohuoside I Inhibits the Proliferation of Pancreatic Cancer Cells via mTOR/S6K1-Caspases/Bcl2/Bax Apoptotic Signaling |
title_sort | baohuoside i inhibits the proliferation of pancreatic cancer cells via mtor/s6k1-caspases/bcl2/bax apoptotic signaling |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6927568/ https://www.ncbi.nlm.nih.gov/pubmed/31908533 http://dx.doi.org/10.2147/CMAR.S228926 |
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