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Urushiol Induces Apoptosis via a p53-dependent Pathway in Human Gastric Cancer Cells
BACKGROUND: Urushiols are mixtures of olefinic catechols which is isolated from the sap of Korean lacquer tree (Rhus vernicifera Stokes). The aim of this study was to determine the anticancer effects of urushiol in human gastric adenocarcinoma cell lines. METHODS: The cytotoxicity of urushiols was a...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Korean Society of Cancer Prevention
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4189456/ https://www.ncbi.nlm.nih.gov/pubmed/25337543 http://dx.doi.org/10.15430/JCP.2013.18.2.169 |
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author | Kim, Seaho Kim, Dong Hwan Lee, Sun Hwa Kim, Min Jeong Yoon, Jeong-Hyun Chung, Hae Young Na, Chun Soo Kim, Nam Deuk |
author_facet | Kim, Seaho Kim, Dong Hwan Lee, Sun Hwa Kim, Min Jeong Yoon, Jeong-Hyun Chung, Hae Young Na, Chun Soo Kim, Nam Deuk |
author_sort | Kim, Seaho |
collection | PubMed |
description | BACKGROUND: Urushiols are mixtures of olefinic catechols which is isolated from the sap of Korean lacquer tree (Rhus vernicifera Stokes). The aim of this study was to determine the anticancer effects of urushiol in human gastric adenocarcinoma cell lines. METHODS: The cytotoxicity of urushiols was assessed by MTT assays on the two gastric adenocarcinoma cell lines, MKN-45 (wild type of p53) and MKN-28 (mutant type of p53). We also examined the action mechanisms of urushiol by analyzing its effects on cell cycle progression and apoptosis induction. RESULTS: The cytotoxic results from MTT assays indicated that urushiol inhibited human gastric cancer cell growth in a dose-dependent manner, with IC50 values of approximately 15 and 20 μg/ml on MKN-45 and MKN-28 cells, respectively. Urushiol mediated cell death on these two cancer cell lines through different pathways. Urushiol induced apoptosis on MKN-45 cells, concomitant with apoptotic nuclear change, DNA fragmentation, poly (ADP-ribose) polymerase cleavage and apoptotic body formation via extrinsic pathway of apoptosis. However, no apoptotic features were induced by urushiol treatment on MKN-28 cells. Urushiol induced cytostatic cell growth inhibition via upregulation of the cyclin-dependent kinase inhibitors, p21(WAF1/CIP1) and p27(KIP1) proteins and down-regulation of cyclin-dependent kinase 2 and 4 proteins in a p53-independent manner. CONCLUSIONS: These data provide evidence that urushiol has the potential to be used as a chemotherapeutic agent in human gastric cancer. |
format | Online Article Text |
id | pubmed-4189456 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Korean Society of Cancer Prevention |
record_format | MEDLINE/PubMed |
spelling | pubmed-41894562014-10-21 Urushiol Induces Apoptosis via a p53-dependent Pathway in Human Gastric Cancer Cells Kim, Seaho Kim, Dong Hwan Lee, Sun Hwa Kim, Min Jeong Yoon, Jeong-Hyun Chung, Hae Young Na, Chun Soo Kim, Nam Deuk J Cancer Prev Original Article BACKGROUND: Urushiols are mixtures of olefinic catechols which is isolated from the sap of Korean lacquer tree (Rhus vernicifera Stokes). The aim of this study was to determine the anticancer effects of urushiol in human gastric adenocarcinoma cell lines. METHODS: The cytotoxicity of urushiols was assessed by MTT assays on the two gastric adenocarcinoma cell lines, MKN-45 (wild type of p53) and MKN-28 (mutant type of p53). We also examined the action mechanisms of urushiol by analyzing its effects on cell cycle progression and apoptosis induction. RESULTS: The cytotoxic results from MTT assays indicated that urushiol inhibited human gastric cancer cell growth in a dose-dependent manner, with IC50 values of approximately 15 and 20 μg/ml on MKN-45 and MKN-28 cells, respectively. Urushiol mediated cell death on these two cancer cell lines through different pathways. Urushiol induced apoptosis on MKN-45 cells, concomitant with apoptotic nuclear change, DNA fragmentation, poly (ADP-ribose) polymerase cleavage and apoptotic body formation via extrinsic pathway of apoptosis. However, no apoptotic features were induced by urushiol treatment on MKN-28 cells. Urushiol induced cytostatic cell growth inhibition via upregulation of the cyclin-dependent kinase inhibitors, p21(WAF1/CIP1) and p27(KIP1) proteins and down-regulation of cyclin-dependent kinase 2 and 4 proteins in a p53-independent manner. CONCLUSIONS: These data provide evidence that urushiol has the potential to be used as a chemotherapeutic agent in human gastric cancer. Korean Society of Cancer Prevention 2013-06 /pmc/articles/PMC4189456/ /pubmed/25337543 http://dx.doi.org/10.15430/JCP.2013.18.2.169 Text en Copyright © 2013 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/3.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Kim, Seaho Kim, Dong Hwan Lee, Sun Hwa Kim, Min Jeong Yoon, Jeong-Hyun Chung, Hae Young Na, Chun Soo Kim, Nam Deuk Urushiol Induces Apoptosis via a p53-dependent Pathway in Human Gastric Cancer Cells |
title | Urushiol Induces Apoptosis via a p53-dependent Pathway in Human Gastric Cancer Cells |
title_full | Urushiol Induces Apoptosis via a p53-dependent Pathway in Human Gastric Cancer Cells |
title_fullStr | Urushiol Induces Apoptosis via a p53-dependent Pathway in Human Gastric Cancer Cells |
title_full_unstemmed | Urushiol Induces Apoptosis via a p53-dependent Pathway in Human Gastric Cancer Cells |
title_short | Urushiol Induces Apoptosis via a p53-dependent Pathway in Human Gastric Cancer Cells |
title_sort | urushiol induces apoptosis via a p53-dependent pathway in human gastric cancer cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4189456/ https://www.ncbi.nlm.nih.gov/pubmed/25337543 http://dx.doi.org/10.15430/JCP.2013.18.2.169 |
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