Reduced CTGF expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.

<h4>Background</h4>The role of CTGF varies in different types of cancer. The purpose of this study is to investigate the involvement of CTGF in tumor progression and prognosis of human nasopharyngeal carcinoma (NPC).<h4>Experimental design</h4>CTGF expression levels were exam...

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Autores principales: Yan Zhen, Yanfen Ye, Xiaoli Yu, Chunping Mai, Ying Zhou, Yan Chen, Huiling Yang, Xiaoming Lyu, Ye Song, Qiangyun Wu, Qiaofen Fu, Mengyang Zhao, Shengni Hua, Hao Wang, Zhen Liu, Yajie Zhang, Weiyi Fang
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Publicado: Public Library of Science (PLoS) 2014
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spelling oai:doaj.org-article:b8fff61713ba4587b39030e6016f34852021-11-18T07:43:15ZReduced CTGF expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.1932-620310.1371/journal.pone.0064976https://doaj.org/article/b8fff61713ba4587b39030e6016f34852014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23755163/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>The role of CTGF varies in different types of cancer. The purpose of this study is to investigate the involvement of CTGF in tumor progression and prognosis of human nasopharyngeal carcinoma (NPC).<h4>Experimental design</h4>CTGF expression levels were examined in NPC tissues and cells, nasopharynx (NP) tissues, and NP69 cells. The effects and molecular mechanisms of CTGF expression on cell proliferation, migration, invasion, and cell cycle were also explored.<h4>Results</h4>NPC cells exhibited decreased mRNA expression of CTGF compared to immortalized human nasopharyngeal epithelial cell line NP69. Similarly, CTGF was observed to be downregulated in NPC compared to normal tissues at mRNA and protein levels. Furthermore, reduced CTGF was negatively associated with the progression of NPC. Knocking down CTGF expression enhanced the colony formation, cell migration, invasion, and G1/S cell cycle transition. Mechanistic analysis revealed that CTGF suppression activated FAK/PI3K/AKT and its downstream signals regulating the cell cycle, epithelial-mesenchymal transition (EMT) and MMPs. Finally, DNA methylation microarray revealed a lack of hypermethylation at the CTGF promoter, suggesting other mechanisms are associated with suppression of CTGF in NPC.<h4>Conclusion</h4>Our study demonstrates that reduced expression of CTGF promoted cell proliferation, migration, invasion and cell cycle progression through FAK/PI3K/AKT, EMT and MMP pathways in NPC.Yan ZhenYanfen YeXiaoli YuChunping MaiYing ZhouYan ChenHuiling YangXiaoming LyuYe SongQiangyun WuQiaofen FuMengyang ZhaoShengni HuaHao WangZhen LiuYajie ZhangWeiyi FangPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 6, p e64976 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Yan Zhen
Yanfen Ye
Xiaoli Yu
Chunping Mai
Ying Zhou
Yan Chen
Huiling Yang
Xiaoming Lyu
Ye Song
Qiangyun Wu
Qiaofen Fu
Mengyang Zhao
Shengni Hua
Hao Wang
Zhen Liu
Yajie Zhang
Weiyi Fang
Reduced CTGF expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.
description <h4>Background</h4>The role of CTGF varies in different types of cancer. The purpose of this study is to investigate the involvement of CTGF in tumor progression and prognosis of human nasopharyngeal carcinoma (NPC).<h4>Experimental design</h4>CTGF expression levels were examined in NPC tissues and cells, nasopharynx (NP) tissues, and NP69 cells. The effects and molecular mechanisms of CTGF expression on cell proliferation, migration, invasion, and cell cycle were also explored.<h4>Results</h4>NPC cells exhibited decreased mRNA expression of CTGF compared to immortalized human nasopharyngeal epithelial cell line NP69. Similarly, CTGF was observed to be downregulated in NPC compared to normal tissues at mRNA and protein levels. Furthermore, reduced CTGF was negatively associated with the progression of NPC. Knocking down CTGF expression enhanced the colony formation, cell migration, invasion, and G1/S cell cycle transition. Mechanistic analysis revealed that CTGF suppression activated FAK/PI3K/AKT and its downstream signals regulating the cell cycle, epithelial-mesenchymal transition (EMT) and MMPs. Finally, DNA methylation microarray revealed a lack of hypermethylation at the CTGF promoter, suggesting other mechanisms are associated with suppression of CTGF in NPC.<h4>Conclusion</h4>Our study demonstrates that reduced expression of CTGF promoted cell proliferation, migration, invasion and cell cycle progression through FAK/PI3K/AKT, EMT and MMP pathways in NPC.
format article
author Yan Zhen
Yanfen Ye
Xiaoli Yu
Chunping Mai
Ying Zhou
Yan Chen
Huiling Yang
Xiaoming Lyu
Ye Song
Qiangyun Wu
Qiaofen Fu
Mengyang Zhao
Shengni Hua
Hao Wang
Zhen Liu
Yajie Zhang
Weiyi Fang
author_facet Yan Zhen
Yanfen Ye
Xiaoli Yu
Chunping Mai
Ying Zhou
Yan Chen
Huiling Yang
Xiaoming Lyu
Ye Song
Qiangyun Wu
Qiaofen Fu
Mengyang Zhao
Shengni Hua
Hao Wang
Zhen Liu
Yajie Zhang
Weiyi Fang
author_sort Yan Zhen
title Reduced CTGF expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.
title_short Reduced CTGF expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.
title_full Reduced CTGF expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.
title_fullStr Reduced CTGF expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.
title_full_unstemmed Reduced CTGF expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.
title_sort reduced ctgf expression promotes cell growth, migration, and invasion in nasopharyngeal carcinoma.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/b8fff61713ba4587b39030e6016f3485
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