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The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines

OBJECTIVES: The purpose of this study was to evaluate the anti-cancer activity of cisplatin by studying its effects on cell viability and identifying the mechanisms underlying the induction of cell cycle arrest and apoptosis on oral squamous cell carcinoma (OSCC) cell lines with varying p53 mutation...

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Autores principales: Jo, Deuk-Won, Kim, Young-Kyun, Yun, Pil-Young
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Association of Oral and Maxillofacial Surgeons 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5206238/
https://www.ncbi.nlm.nih.gov/pubmed/28053903
http://dx.doi.org/10.5125/jkaoms.2016.42.6.337
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author Jo, Deuk-Won
Kim, Young-Kyun
Yun, Pil-Young
author_facet Jo, Deuk-Won
Kim, Young-Kyun
Yun, Pil-Young
author_sort Jo, Deuk-Won
collection PubMed
description OBJECTIVES: The purpose of this study was to evaluate the anti-cancer activity of cisplatin by studying its effects on cell viability and identifying the mechanisms underlying the induction of cell cycle arrest and apoptosis on oral squamous cell carcinoma (OSCC) cell lines with varying p53 mutation status. MATERIALS AND METHODS: Three OSCC cell lines, YD-8 (p53 point mutation), YD-9 (p53 wild type), and YD-38 (p53 deletion) were used. To determine the cytotoxic effect of cisplatin, MTS assay was performed. The cell cycle alteration and apoptosis were analyzed using flow cytometry. Western blot analysis was used to detect the expression of cell cycle alteration- or apoptosis-related proteins as well as p53. RESULTS: Cisplatin showed a time- and dose-dependent anti-proliferative effect in all cell lines. Cisplatin induced G2/M cell accumulation in the three cell lines after treatment with 0.5 and 1.0 µg/mL of cisplatin for 48 hours. The proportion of annexin V-FITC-stained cells increased following treatment with cisplatin. The apoptotic proportion was lower in the YD-38 cell line than in the YD-9 or YD-8 cell lines. Also, immunoblotting analysis indicated that p53 and p21 were detected only in YD-8 and YD-9 cell lines after cisplatin treatment. CONCLUSION: In this study, cisplatin showed anti-cancer effects via G2/M phase arrest and apoptosis, with some difference among OSCC cell lines. The mutation status of p53 might have influenced the difference observed among cell lines. Further studies on p53 mutation status are needed to understand the biological behavior and characteristics of OSCCs and to establish appropriate treatment.
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spelling pubmed-52062382017-01-04 The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines Jo, Deuk-Won Kim, Young-Kyun Yun, Pil-Young J Korean Assoc Oral Maxillofac Surg Original Article OBJECTIVES: The purpose of this study was to evaluate the anti-cancer activity of cisplatin by studying its effects on cell viability and identifying the mechanisms underlying the induction of cell cycle arrest and apoptosis on oral squamous cell carcinoma (OSCC) cell lines with varying p53 mutation status. MATERIALS AND METHODS: Three OSCC cell lines, YD-8 (p53 point mutation), YD-9 (p53 wild type), and YD-38 (p53 deletion) were used. To determine the cytotoxic effect of cisplatin, MTS assay was performed. The cell cycle alteration and apoptosis were analyzed using flow cytometry. Western blot analysis was used to detect the expression of cell cycle alteration- or apoptosis-related proteins as well as p53. RESULTS: Cisplatin showed a time- and dose-dependent anti-proliferative effect in all cell lines. Cisplatin induced G2/M cell accumulation in the three cell lines after treatment with 0.5 and 1.0 µg/mL of cisplatin for 48 hours. The proportion of annexin V-FITC-stained cells increased following treatment with cisplatin. The apoptotic proportion was lower in the YD-38 cell line than in the YD-9 or YD-8 cell lines. Also, immunoblotting analysis indicated that p53 and p21 were detected only in YD-8 and YD-9 cell lines after cisplatin treatment. CONCLUSION: In this study, cisplatin showed anti-cancer effects via G2/M phase arrest and apoptosis, with some difference among OSCC cell lines. The mutation status of p53 might have influenced the difference observed among cell lines. Further studies on p53 mutation status are needed to understand the biological behavior and characteristics of OSCCs and to establish appropriate treatment. The Korean Association of Oral and Maxillofacial Surgeons 2016-12 2016-12-27 /pmc/articles/PMC5206238/ /pubmed/28053903 http://dx.doi.org/10.5125/jkaoms.2016.42.6.337 Text en Copyright © 2016 The Korean Association of Oral and Maxillofacial Surgeons. All rights reserved. http://creativecommons.org/licenses/by-nc/4.0/ 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
Jo, Deuk-Won
Kim, Young-Kyun
Yun, Pil-Young
The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines
title The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines
title_full The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines
title_fullStr The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines
title_full_unstemmed The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines
title_short The influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines
title_sort influence of p53 mutation status on the anti-cancer effect of cisplatin in oral squamous cell carcinoma cell lines
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5206238/
https://www.ncbi.nlm.nih.gov/pubmed/28053903
http://dx.doi.org/10.5125/jkaoms.2016.42.6.337
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