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Ursodeoxycholic Acid Induces Death Receptor-mediated Apoptosis in Prostate Cancer Cells
BACKGROUND: Bile acids have anti-cancer properties in a certain types of cancers. We determined anticancer activity and its underlying molecular mechanism of ursodeoxycholic acid (UDCA) in human DU145 prostate cancer cells. METHODS: Cell viability was measured with an MTT assay. UDCA-induced apoptos...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean Society of Cancer Prevention
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380185/ https://www.ncbi.nlm.nih.gov/pubmed/28382282 http://dx.doi.org/10.15430/JCP.2017.22.1.16 |
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author | Lee, Won Sup Jung, Ji Hyun Panchanathan, Radha Yun, Jeong Won Kim, Dong Hoon Kim, Hye Jung Kim, Gon Sup Ryu, Chung Ho Shin, Sung Chul Hong, Soon Chan Choi, Yung Hyun Jung, Jin-Myung |
author_facet | Lee, Won Sup Jung, Ji Hyun Panchanathan, Radha Yun, Jeong Won Kim, Dong Hoon Kim, Hye Jung Kim, Gon Sup Ryu, Chung Ho Shin, Sung Chul Hong, Soon Chan Choi, Yung Hyun Jung, Jin-Myung |
author_sort | Lee, Won Sup |
collection | PubMed |
description | BACKGROUND: Bile acids have anti-cancer properties in a certain types of cancers. We determined anticancer activity and its underlying molecular mechanism of ursodeoxycholic acid (UDCA) in human DU145 prostate cancer cells. METHODS: Cell viability was measured with an MTT assay. UDCA-induced apoptosis was determined with flow cytometric analysis. The expression levels of apoptosis-related signaling proteins were examined with Western blotting. RESULTS: UDCA treatment significantly inhibited cell growth of DU145 in a dose-dependent manner. It induced cellular shrinkage and cytoplasmic blebs and accumulated the cells with sub-G1 DNA contents. Moreover, UDCA activated caspase 8, suggesting that UDCA-induced apoptosis is associated with extrinsic pathway. Consistent to this finding, UDCA increased the expressions of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor, death receptor 4 (DR4) and death receptor 5 (DR5), and TRAIL augmented the UDCA-induced cell death in DU145 cells. In addition, UDCA also increased the expressions of Bax and cytochrome c and decreased the expression of Bcl-xL in DU145 cells. This finding suggests that UDCA-induced apoptosis may be involved in intrinsic pathway. CONCLUSIONS: UDCA induces apoptosis via extrinsic pathway as well as intrinsic pathway in DU145 prostate cancer cells. UDCA may be a promising anti-cancer agent against prostate cancer. |
format | Online Article Text |
id | pubmed-5380185 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Korean Society of Cancer Prevention |
record_format | MEDLINE/PubMed |
spelling | pubmed-53801852017-04-05 Ursodeoxycholic Acid Induces Death Receptor-mediated Apoptosis in Prostate Cancer Cells Lee, Won Sup Jung, Ji Hyun Panchanathan, Radha Yun, Jeong Won Kim, Dong Hoon Kim, Hye Jung Kim, Gon Sup Ryu, Chung Ho Shin, Sung Chul Hong, Soon Chan Choi, Yung Hyun Jung, Jin-Myung J Cancer Prev Original Article BACKGROUND: Bile acids have anti-cancer properties in a certain types of cancers. We determined anticancer activity and its underlying molecular mechanism of ursodeoxycholic acid (UDCA) in human DU145 prostate cancer cells. METHODS: Cell viability was measured with an MTT assay. UDCA-induced apoptosis was determined with flow cytometric analysis. The expression levels of apoptosis-related signaling proteins were examined with Western blotting. RESULTS: UDCA treatment significantly inhibited cell growth of DU145 in a dose-dependent manner. It induced cellular shrinkage and cytoplasmic blebs and accumulated the cells with sub-G1 DNA contents. Moreover, UDCA activated caspase 8, suggesting that UDCA-induced apoptosis is associated with extrinsic pathway. Consistent to this finding, UDCA increased the expressions of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor, death receptor 4 (DR4) and death receptor 5 (DR5), and TRAIL augmented the UDCA-induced cell death in DU145 cells. In addition, UDCA also increased the expressions of Bax and cytochrome c and decreased the expression of Bcl-xL in DU145 cells. This finding suggests that UDCA-induced apoptosis may be involved in intrinsic pathway. CONCLUSIONS: UDCA induces apoptosis via extrinsic pathway as well as intrinsic pathway in DU145 prostate cancer cells. UDCA may be a promising anti-cancer agent against prostate cancer. Korean Society of Cancer Prevention 2017-03 2017-03-30 /pmc/articles/PMC5380185/ /pubmed/28382282 http://dx.doi.org/10.15430/JCP.2017.22.1.16 Text en Copyright © 2017 Korean Society of Cancer Prevention This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://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 | Original Article Lee, Won Sup Jung, Ji Hyun Panchanathan, Radha Yun, Jeong Won Kim, Dong Hoon Kim, Hye Jung Kim, Gon Sup Ryu, Chung Ho Shin, Sung Chul Hong, Soon Chan Choi, Yung Hyun Jung, Jin-Myung Ursodeoxycholic Acid Induces Death Receptor-mediated Apoptosis in Prostate Cancer Cells |
title | Ursodeoxycholic Acid Induces Death Receptor-mediated Apoptosis in Prostate Cancer Cells |
title_full | Ursodeoxycholic Acid Induces Death Receptor-mediated Apoptosis in Prostate Cancer Cells |
title_fullStr | Ursodeoxycholic Acid Induces Death Receptor-mediated Apoptosis in Prostate Cancer Cells |
title_full_unstemmed | Ursodeoxycholic Acid Induces Death Receptor-mediated Apoptosis in Prostate Cancer Cells |
title_short | Ursodeoxycholic Acid Induces Death Receptor-mediated Apoptosis in Prostate Cancer Cells |
title_sort | ursodeoxycholic acid induces death receptor-mediated apoptosis in prostate cancer cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5380185/ https://www.ncbi.nlm.nih.gov/pubmed/28382282 http://dx.doi.org/10.15430/JCP.2017.22.1.16 |
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