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Silencing of c-jun decreases cell migration, invasion, and EMT in radioresistant human nasopharyngeal carcinoma cell line CNE-2R
BACKGROUND: Previously, we found that c-jun was highly expressed in radiation-resistant human nasopharyngeal carcinoma cells (CNE-2R) compared with human nasopharyngeal carcinoma cells (CNE-2). MATERIALS AND METHODS: In this study, we first used the scratch assays and transwell assays to detect the...
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/PMC6038861/ https://www.ncbi.nlm.nih.gov/pubmed/30013361 http://dx.doi.org/10.2147/OTT.S162700 |
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author | Lin, Guoxiang Yu, Binbin Liang, Zhongguo Li, Ling Qu, Song Chen, Kaihua Zhou, Lei Lu, Qiteng Sun, Yongchu Zhu, Xiaodong |
author_facet | Lin, Guoxiang Yu, Binbin Liang, Zhongguo Li, Ling Qu, Song Chen, Kaihua Zhou, Lei Lu, Qiteng Sun, Yongchu Zhu, Xiaodong |
author_sort | Lin, Guoxiang |
collection | PubMed |
description | BACKGROUND: Previously, we found that c-jun was highly expressed in radiation-resistant human nasopharyngeal carcinoma cells (CNE-2R) compared with human nasopharyngeal carcinoma cells (CNE-2). MATERIALS AND METHODS: In this study, we first used the scratch assays and transwell assays to detect the migration and invasion of CNE-2R and CNE-2 cells and tested the epithelial mesenchymal transformation (EMT)-related proteins E-cadherin and N-cadherin by Western blot analysis. Subsequently, c-jun was knocked down to establish the effect of c-jun on EMT, migration, and invasion of CNE-2R cells both in vitro and in vivo. RESULTS: A high EMT level, CNE-2R cells were more capable of migration and invasion than CNE-2 cells. Moreover, silencing of c-jun has upregulated the expression of E-cadherin and downregulated N-cadherin in CNE-2R cells, and subsequently the migration and invasion capacity of the cells was decreased. Consistent with in vitro results, in vivo studies indicated that the c-jun silencing reduced pulmonary migration of CNE-2R cells. Immunohistochemistry of lung metastatic tumor tissue showed that E-cadherin was upregulated, and N-cadherin was downregulated. CONCLUSION: These findings suggest that silencing of c-jun in CNE-2R cells reduces cells migration, invasion, and EMT both in vitro and in vivo. |
format | Online Article Text |
id | pubmed-6038861 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-60388612018-07-16 Silencing of c-jun decreases cell migration, invasion, and EMT in radioresistant human nasopharyngeal carcinoma cell line CNE-2R Lin, Guoxiang Yu, Binbin Liang, Zhongguo Li, Ling Qu, Song Chen, Kaihua Zhou, Lei Lu, Qiteng Sun, Yongchu Zhu, Xiaodong Onco Targets Ther Original Research BACKGROUND: Previously, we found that c-jun was highly expressed in radiation-resistant human nasopharyngeal carcinoma cells (CNE-2R) compared with human nasopharyngeal carcinoma cells (CNE-2). MATERIALS AND METHODS: In this study, we first used the scratch assays and transwell assays to detect the migration and invasion of CNE-2R and CNE-2 cells and tested the epithelial mesenchymal transformation (EMT)-related proteins E-cadherin and N-cadherin by Western blot analysis. Subsequently, c-jun was knocked down to establish the effect of c-jun on EMT, migration, and invasion of CNE-2R cells both in vitro and in vivo. RESULTS: A high EMT level, CNE-2R cells were more capable of migration and invasion than CNE-2 cells. Moreover, silencing of c-jun has upregulated the expression of E-cadherin and downregulated N-cadherin in CNE-2R cells, and subsequently the migration and invasion capacity of the cells was decreased. Consistent with in vitro results, in vivo studies indicated that the c-jun silencing reduced pulmonary migration of CNE-2R cells. Immunohistochemistry of lung metastatic tumor tissue showed that E-cadherin was upregulated, and N-cadherin was downregulated. CONCLUSION: These findings suggest that silencing of c-jun in CNE-2R cells reduces cells migration, invasion, and EMT both in vitro and in vivo. Dove Medical Press 2018-07-04 /pmc/articles/PMC6038861/ /pubmed/30013361 http://dx.doi.org/10.2147/OTT.S162700 Text en © 2018 Lin 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 Lin, Guoxiang Yu, Binbin Liang, Zhongguo Li, Ling Qu, Song Chen, Kaihua Zhou, Lei Lu, Qiteng Sun, Yongchu Zhu, Xiaodong Silencing of c-jun decreases cell migration, invasion, and EMT in radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title | Silencing of c-jun decreases cell migration, invasion, and EMT in radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_full | Silencing of c-jun decreases cell migration, invasion, and EMT in radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_fullStr | Silencing of c-jun decreases cell migration, invasion, and EMT in radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_full_unstemmed | Silencing of c-jun decreases cell migration, invasion, and EMT in radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_short | Silencing of c-jun decreases cell migration, invasion, and EMT in radioresistant human nasopharyngeal carcinoma cell line CNE-2R |
title_sort | silencing of c-jun decreases cell migration, invasion, and emt in radioresistant human nasopharyngeal carcinoma cell line cne-2r |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6038861/ https://www.ncbi.nlm.nih.gov/pubmed/30013361 http://dx.doi.org/10.2147/OTT.S162700 |
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