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A high bile acid environment promotes apoptosis and inhibits migration in pancreatic cancer

Bile acids, the main organic solutes in bile, have been established to play an important role at physiological concentrations in gastrointestinal metabolism. However, under pathological conditions, such as cholestatic disease, cholestasis can damage hepatocytes/biliary epithelial cells leading to ap...

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Autores principales: Zhu, Shaopu, Yang, Kang, Yang, Shiyi, Zhang, Li, Xiong, Maoming, Zhang, Jiawei, Chen, Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8973854/
https://www.ncbi.nlm.nih.gov/pubmed/35245979
http://dx.doi.org/10.1080/21655979.2022.2045823
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author Zhu, Shaopu
Yang, Kang
Yang, Shiyi
Zhang, Li
Xiong, Maoming
Zhang, Jiawei
Chen, Bo
author_facet Zhu, Shaopu
Yang, Kang
Yang, Shiyi
Zhang, Li
Xiong, Maoming
Zhang, Jiawei
Chen, Bo
author_sort Zhu, Shaopu
collection PubMed
description Bile acids, the main organic solutes in bile, have been established to play an important role at physiological concentrations in gastrointestinal metabolism. However, under pathological conditions, such as cholestatic disease, cholestasis can damage hepatocytes/biliary epithelial cells leading to apoptosis or necrosis. Clinically, pancreatic head cancer usually presents with obstructive jaundice and increased serum bile acid levels, suggesting that pancreatic cancer is intricately correlated with a high bile acid environment in the human body. An increasing body of evidence suggests that bile acids are toxic to normal human and colon cancer cells. Nonetheless, the effect of bile acids on the occurrence and development of pancreatic cancer remains a matter of debate. In the present study, to explore the direct effects of high serum concentrations of bile acids on pancreatic cancer and the possible related mechanisms, human pancreatic cancer (PANC-1) cells were subject to different concentrations of bile acid mixtures to assess cell viability and the migration and invasion ability. Besides, we found that a high bile acid environment could inhibit the proliferation and migration of pancreatic cancer cells through ROS(Reactive oxygen species) induction and the EMT(epithelial-mesenchymal transition) pathway, thereby promoting the apoptosis of pancreatic cancer cells. Abbreviations BAs: Bile Acids; EMT: epithelial-mesenchymal transition; FBS: fatal bovine serum;CCK-8: Cell-Counting-Kit-8; ROS: reactive oxygen species; CA: cholic acid; CDCA: chenodeoxycholic acid; GCDCA: Glycochenodeoxycholic acid; PVDF: Poly vinylidene fluoride
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spelling pubmed-89738542022-04-02 A high bile acid environment promotes apoptosis and inhibits migration in pancreatic cancer Zhu, Shaopu Yang, Kang Yang, Shiyi Zhang, Li Xiong, Maoming Zhang, Jiawei Chen, Bo Bioengineered Research Paper Bile acids, the main organic solutes in bile, have been established to play an important role at physiological concentrations in gastrointestinal metabolism. However, under pathological conditions, such as cholestatic disease, cholestasis can damage hepatocytes/biliary epithelial cells leading to apoptosis or necrosis. Clinically, pancreatic head cancer usually presents with obstructive jaundice and increased serum bile acid levels, suggesting that pancreatic cancer is intricately correlated with a high bile acid environment in the human body. An increasing body of evidence suggests that bile acids are toxic to normal human and colon cancer cells. Nonetheless, the effect of bile acids on the occurrence and development of pancreatic cancer remains a matter of debate. In the present study, to explore the direct effects of high serum concentrations of bile acids on pancreatic cancer and the possible related mechanisms, human pancreatic cancer (PANC-1) cells were subject to different concentrations of bile acid mixtures to assess cell viability and the migration and invasion ability. Besides, we found that a high bile acid environment could inhibit the proliferation and migration of pancreatic cancer cells through ROS(Reactive oxygen species) induction and the EMT(epithelial-mesenchymal transition) pathway, thereby promoting the apoptosis of pancreatic cancer cells. Abbreviations BAs: Bile Acids; EMT: epithelial-mesenchymal transition; FBS: fatal bovine serum;CCK-8: Cell-Counting-Kit-8; ROS: reactive oxygen species; CA: cholic acid; CDCA: chenodeoxycholic acid; GCDCA: Glycochenodeoxycholic acid; PVDF: Poly vinylidene fluoride Taylor & Francis 2022-03-04 /pmc/articles/PMC8973854/ /pubmed/35245979 http://dx.doi.org/10.1080/21655979.2022.2045823 Text en © 2022 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. https://creativecommons.org/licenses/by-nc/4.0/This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) ), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Zhu, Shaopu
Yang, Kang
Yang, Shiyi
Zhang, Li
Xiong, Maoming
Zhang, Jiawei
Chen, Bo
A high bile acid environment promotes apoptosis and inhibits migration in pancreatic cancer
title A high bile acid environment promotes apoptosis and inhibits migration in pancreatic cancer
title_full A high bile acid environment promotes apoptosis and inhibits migration in pancreatic cancer
title_fullStr A high bile acid environment promotes apoptosis and inhibits migration in pancreatic cancer
title_full_unstemmed A high bile acid environment promotes apoptosis and inhibits migration in pancreatic cancer
title_short A high bile acid environment promotes apoptosis and inhibits migration in pancreatic cancer
title_sort high bile acid environment promotes apoptosis and inhibits migration in pancreatic cancer
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8973854/
https://www.ncbi.nlm.nih.gov/pubmed/35245979
http://dx.doi.org/10.1080/21655979.2022.2045823
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