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Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS
Glutaredoxin 3 (GLRX3) is antioxidant enzyme, maintaining a low level of ROS, thus contributing to the survival and metastasis of several types of cancer. However, the expression and functions of GLRX3 have not been addressed in nasopharyngeal carcinoma (NPC). In this study, we found that GLRX3 was...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5095054/ https://www.ncbi.nlm.nih.gov/pubmed/27203742 http://dx.doi.org/10.18632/oncotarget.9454 |
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author | He, Feng Wei, Lili Luo, Wenqi Liao, Zhipeng Li, Bo Zhou, Xiaoying Xiao, Xue You, Jingping Chen, Yufeng Zheng, Shixing Li, Ping Murata, Mariko Huang, Guangwu Zhang, Zhe |
author_facet | He, Feng Wei, Lili Luo, Wenqi Liao, Zhipeng Li, Bo Zhou, Xiaoying Xiao, Xue You, Jingping Chen, Yufeng Zheng, Shixing Li, Ping Murata, Mariko Huang, Guangwu Zhang, Zhe |
author_sort | He, Feng |
collection | PubMed |
description | Glutaredoxin 3 (GLRX3) is antioxidant enzyme, maintaining a low level of ROS, thus contributing to the survival and metastasis of several types of cancer. However, the expression and functions of GLRX3 have not been addressed in nasopharyngeal carcinoma (NPC). In this study, we found that GLRX3 was overexpressed in NPC. Knockdown of GLRX3 in NPC cell lines inhibited proliferation in vitro, tumorignesis in vivo, and colony formation. In addition, GLRX3 knockdown decreased the migration and invasion capacity of NPC cells by reversing the epithelial-mesenchymal transition (EMT). Furthermore, stabilization of GLRX3 was positively related to with epidermal growth factor receptor (EGFR) expression and negatively with ROS generation. Phosphorylation of Akt, a key downstream effector, was induced by EGFR signaling but did not rely on increasing ROS level in NPC cells. GLRX3 might be an oncoprotein in NPC, playing important roles in increasing redox reaction and activating EGFR/ Akt signals, so it may be a therapeutic target for NPC. |
format | Online Article Text |
id | pubmed-5095054 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-50950542016-11-22 Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS He, Feng Wei, Lili Luo, Wenqi Liao, Zhipeng Li, Bo Zhou, Xiaoying Xiao, Xue You, Jingping Chen, Yufeng Zheng, Shixing Li, Ping Murata, Mariko Huang, Guangwu Zhang, Zhe Oncotarget Research Paper Glutaredoxin 3 (GLRX3) is antioxidant enzyme, maintaining a low level of ROS, thus contributing to the survival and metastasis of several types of cancer. However, the expression and functions of GLRX3 have not been addressed in nasopharyngeal carcinoma (NPC). In this study, we found that GLRX3 was overexpressed in NPC. Knockdown of GLRX3 in NPC cell lines inhibited proliferation in vitro, tumorignesis in vivo, and colony formation. In addition, GLRX3 knockdown decreased the migration and invasion capacity of NPC cells by reversing the epithelial-mesenchymal transition (EMT). Furthermore, stabilization of GLRX3 was positively related to with epidermal growth factor receptor (EGFR) expression and negatively with ROS generation. Phosphorylation of Akt, a key downstream effector, was induced by EGFR signaling but did not rely on increasing ROS level in NPC cells. GLRX3 might be an oncoprotein in NPC, playing important roles in increasing redox reaction and activating EGFR/ Akt signals, so it may be a therapeutic target for NPC. Impact Journals LLC 2016-05-18 /pmc/articles/PMC5095054/ /pubmed/27203742 http://dx.doi.org/10.18632/oncotarget.9454 Text en Copyright: © 2016 He et al. http://creativecommons.org/licenses/by/2.5/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper He, Feng Wei, Lili Luo, Wenqi Liao, Zhipeng Li, Bo Zhou, Xiaoying Xiao, Xue You, Jingping Chen, Yufeng Zheng, Shixing Li, Ping Murata, Mariko Huang, Guangwu Zhang, Zhe Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS |
title | Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS |
title_full | Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS |
title_fullStr | Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS |
title_full_unstemmed | Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS |
title_short | Glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via EGFR/Akt pathway and independent of ROS |
title_sort | glutaredoxin 3 promotes nasopharyngeal carcinoma growth and metastasis via egfr/akt pathway and independent of ros |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5095054/ https://www.ncbi.nlm.nih.gov/pubmed/27203742 http://dx.doi.org/10.18632/oncotarget.9454 |
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