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Inhibitory Effect of Aspirin on Cholangiocarcinoma Cells
Aspirin and other non-steroidal anti-inflammatory drugs reduce the risk of cancer due to their anti-proliferative and apoptotic effects, which are the important mechanisms for their anti-tumor activity. Here, the effect of aspirin on human cholangiocarcinoma cells (KKU-214) and the underlying mechan...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
West Asia Organization for Cancer Prevention
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5773796/ https://www.ncbi.nlm.nih.gov/pubmed/29172284 http://dx.doi.org/10.22034/APJCP.2017.18.11.3091 |
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author | Boueroy, Parichart Aukkanimart, Ratchadawan Boonmars, Thidarut Sriraj, Pranee Ratanasuwan, Panaratana Juasook, Amornrat Wonkchalee, Nadchanan Vaeteewoottacharn, Kulthida Wongkham, Sopit |
author_facet | Boueroy, Parichart Aukkanimart, Ratchadawan Boonmars, Thidarut Sriraj, Pranee Ratanasuwan, Panaratana Juasook, Amornrat Wonkchalee, Nadchanan Vaeteewoottacharn, Kulthida Wongkham, Sopit |
author_sort | Boueroy, Parichart |
collection | PubMed |
description | Aspirin and other non-steroidal anti-inflammatory drugs reduce the risk of cancer due to their anti-proliferative and apoptotic effects, which are the important mechanisms for their anti-tumor activity. Here, the effect of aspirin on human cholangiocarcinoma cells (KKU-214) and the underlying mechanisms of its action were explored. Cell proliferation was measured by sulforhodamine B (SRB) assay, while cell cycle distribution and apoptosis were determined by flow cytometry. Western blotting was used to explore protein expression underlying molecular mechanisms of anti-cancer treatment of aspirin. Aspirin reduced cell proliferation in a dose- and time-dependent manner, and altered the cell cycle phase distribution of KKU-214 cells by increasing the proportion of cells in the G0/G1 phase and reducing the proportion in the S and G2/M phases. Consistent with its effect on the cell cycle, aspirin also reduced the expression of cyclin D1 and cyclin-dependent kinase 4 (Cdk-4), which are important for G0/G1 cell cycle progression. Treatment with aspirin led to increased induction of apoptosis in a dose-dependent manner. Further analysis of the mechanism underlying the effect of this drug showed that aspirin induced the expression of the tumor-suppressor protein p53 while inhibiting the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2). Correspondingly, the activation of caspase-9 and -3 was also increased. These findings suggest that aspirin causes cell cycle arrest and apoptosis, both of which could contribute to its anti-proliferative effect. |
format | Online Article Text |
id | pubmed-5773796 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | West Asia Organization for Cancer Prevention |
record_format | MEDLINE/PubMed |
spelling | pubmed-57737962018-02-01 Inhibitory Effect of Aspirin on Cholangiocarcinoma Cells Boueroy, Parichart Aukkanimart, Ratchadawan Boonmars, Thidarut Sriraj, Pranee Ratanasuwan, Panaratana Juasook, Amornrat Wonkchalee, Nadchanan Vaeteewoottacharn, Kulthida Wongkham, Sopit Asian Pac J Cancer Prev Research Article Aspirin and other non-steroidal anti-inflammatory drugs reduce the risk of cancer due to their anti-proliferative and apoptotic effects, which are the important mechanisms for their anti-tumor activity. Here, the effect of aspirin on human cholangiocarcinoma cells (KKU-214) and the underlying mechanisms of its action were explored. Cell proliferation was measured by sulforhodamine B (SRB) assay, while cell cycle distribution and apoptosis were determined by flow cytometry. Western blotting was used to explore protein expression underlying molecular mechanisms of anti-cancer treatment of aspirin. Aspirin reduced cell proliferation in a dose- and time-dependent manner, and altered the cell cycle phase distribution of KKU-214 cells by increasing the proportion of cells in the G0/G1 phase and reducing the proportion in the S and G2/M phases. Consistent with its effect on the cell cycle, aspirin also reduced the expression of cyclin D1 and cyclin-dependent kinase 4 (Cdk-4), which are important for G0/G1 cell cycle progression. Treatment with aspirin led to increased induction of apoptosis in a dose-dependent manner. Further analysis of the mechanism underlying the effect of this drug showed that aspirin induced the expression of the tumor-suppressor protein p53 while inhibiting the anti-apoptotic protein B-cell lymphoma-2 (Bcl-2). Correspondingly, the activation of caspase-9 and -3 was also increased. These findings suggest that aspirin causes cell cycle arrest and apoptosis, both of which could contribute to its anti-proliferative effect. West Asia Organization for Cancer Prevention 2017 /pmc/articles/PMC5773796/ /pubmed/29172284 http://dx.doi.org/10.22034/APJCP.2017.18.11.3091 Text en Copyright: © Asian Pacific Journal of Cancer Prevention http://creativecommons.org/licenses/BY-SA/4.0 This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License |
spellingShingle | Research Article Boueroy, Parichart Aukkanimart, Ratchadawan Boonmars, Thidarut Sriraj, Pranee Ratanasuwan, Panaratana Juasook, Amornrat Wonkchalee, Nadchanan Vaeteewoottacharn, Kulthida Wongkham, Sopit Inhibitory Effect of Aspirin on Cholangiocarcinoma Cells |
title | Inhibitory Effect of Aspirin on Cholangiocarcinoma Cells |
title_full | Inhibitory Effect of Aspirin on Cholangiocarcinoma Cells |
title_fullStr | Inhibitory Effect of Aspirin on Cholangiocarcinoma Cells |
title_full_unstemmed | Inhibitory Effect of Aspirin on Cholangiocarcinoma Cells |
title_short | Inhibitory Effect of Aspirin on Cholangiocarcinoma Cells |
title_sort | inhibitory effect of aspirin on cholangiocarcinoma cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5773796/ https://www.ncbi.nlm.nih.gov/pubmed/29172284 http://dx.doi.org/10.22034/APJCP.2017.18.11.3091 |
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