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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...

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Autores principales: Boueroy, Parichart, Aukkanimart, Ratchadawan, Boonmars, Thidarut, Sriraj, Pranee, Ratanasuwan, Panaratana, Juasook, Amornrat, Wonkchalee, Nadchanan, Vaeteewoottacharn, Kulthida, Wongkham, Sopit
Formato: Online Artículo Texto
Lenguaje:English
Publicado: West Asia Organization for Cancer Prevention 2017
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.
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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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