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The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R
PURPOSE: The present study aimed to study the role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R. METHODS: Before being irradiated, CNE-2R cells were treated with the autophagy inhibitor chloroquine diphosphate (CDP) or the autophagy induc...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174314/ https://www.ncbi.nlm.nih.gov/pubmed/30323668 http://dx.doi.org/10.2147/CMAR.S176536 |
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author | Liang, Zhong-Guo Lin, Guo-Xiang Yu, Bin-Bin Su, Fang Li, Ling Qu, Song Zhu, Xiao-Dong |
author_facet | Liang, Zhong-Guo Lin, Guo-Xiang Yu, Bin-Bin Su, Fang Li, Ling Qu, Song Zhu, Xiao-Dong |
author_sort | Liang, Zhong-Guo |
collection | PubMed |
description | PURPOSE: The present study aimed to study the role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R. METHODS: Before being irradiated, CNE-2R cells were treated with the autophagy inhibitor chloroquine diphosphate (CDP) or the autophagy inducer rapamycin (RAPA). Microtubule-associated protein light chain 3 (LC3-II) and p62 were assessed using Western blotting analysis 48 hours after CNE-2R cells were irradiated. The percentage of apoptotic cells was assessed via flow cytometry. CNE-2R cell viability was evaluated using the Cell Counting Kit-8 (CCK8). The radiosensitivity of cells was assessed via clone formation analysis. RESULTS: The level of autophagy in CNE-2R cells improved as the radiation dose increased, reaching the maximum at a dose of 10 Gy. Autophagy was most significantly inhibited by 60 µmol/L CDP in CNE-2R cells, but was obviously enhanced by 100 nmol/L RAPA. Compared with the irradiation (IR) alone group, in the IR + CDP group, autophagy was significantly inhibited, viability was low, the rate of radiation-induced apoptosis was increased, and radiosensitivity was upregulated. In contrast, cells of the IR + RAPA group exhibited greater autophagy, higher viability, a lower rate of radiation-induced apoptosis, and downregulated radiosensitivity. CONCLUSION: The autophagy level is negatively correlated with radiosensitivity for the radio-resistant human nasopharyngeal carcinoma cell line CNE-2R. |
format | Online Article Text |
id | pubmed-6174314 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-61743142018-10-15 The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R Liang, Zhong-Guo Lin, Guo-Xiang Yu, Bin-Bin Su, Fang Li, Ling Qu, Song Zhu, Xiao-Dong Cancer Manag Res Original Research PURPOSE: The present study aimed to study the role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R. METHODS: Before being irradiated, CNE-2R cells were treated with the autophagy inhibitor chloroquine diphosphate (CDP) or the autophagy inducer rapamycin (RAPA). Microtubule-associated protein light chain 3 (LC3-II) and p62 were assessed using Western blotting analysis 48 hours after CNE-2R cells were irradiated. The percentage of apoptotic cells was assessed via flow cytometry. CNE-2R cell viability was evaluated using the Cell Counting Kit-8 (CCK8). The radiosensitivity of cells was assessed via clone formation analysis. RESULTS: The level of autophagy in CNE-2R cells improved as the radiation dose increased, reaching the maximum at a dose of 10 Gy. Autophagy was most significantly inhibited by 60 µmol/L CDP in CNE-2R cells, but was obviously enhanced by 100 nmol/L RAPA. Compared with the irradiation (IR) alone group, in the IR + CDP group, autophagy was significantly inhibited, viability was low, the rate of radiation-induced apoptosis was increased, and radiosensitivity was upregulated. In contrast, cells of the IR + RAPA group exhibited greater autophagy, higher viability, a lower rate of radiation-induced apoptosis, and downregulated radiosensitivity. CONCLUSION: The autophagy level is negatively correlated with radiosensitivity for the radio-resistant human nasopharyngeal carcinoma cell line CNE-2R. Dove Medical Press 2018-10-02 /pmc/articles/PMC6174314/ /pubmed/30323668 http://dx.doi.org/10.2147/CMAR.S176536 Text en © 2018 Liang et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. |
spellingShingle | Original Research Liang, Zhong-Guo Lin, Guo-Xiang Yu, Bin-Bin Su, Fang Li, Ling Qu, Song Zhu, Xiao-Dong The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title | The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_full | The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_fullStr | The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_full_unstemmed | The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_short | The role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_sort | role of autophagy in the radiosensitivity of the radioresistant human nasopharyngeal carcinoma cell line cne-2r |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6174314/ https://www.ncbi.nlm.nih.gov/pubmed/30323668 http://dx.doi.org/10.2147/CMAR.S176536 |
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