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Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis

Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer-related death, especially in China. In addition, the prognosis of late stage patients is extremely poor. However, the biological significance of the long non-coding RNA lnc-ATB and its potential role in ESCC remain to b...

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Autores principales: Li, Zhongwen, Wu, Xiaoliang, Gu, Ling, Shen, Qi, Luo, Wen, Deng, Chuangzhong, Zhou, Qianghua, Chen, Xinru, Li, Yanjie, Lim, ZuanFu, Wang, Xing, Wang, Jiahong, Yang, Xianzi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520904/
https://www.ncbi.nlm.nih.gov/pubmed/28640252
http://dx.doi.org/10.1038/cddis.2017.245
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author Li, Zhongwen
Wu, Xiaoliang
Gu, Ling
Shen, Qi
Luo, Wen
Deng, Chuangzhong
Zhou, Qianghua
Chen, Xinru
Li, Yanjie
Lim, ZuanFu
Wang, Xing
Wang, Jiahong
Yang, Xianzi
author_facet Li, Zhongwen
Wu, Xiaoliang
Gu, Ling
Shen, Qi
Luo, Wen
Deng, Chuangzhong
Zhou, Qianghua
Chen, Xinru
Li, Yanjie
Lim, ZuanFu
Wang, Xing
Wang, Jiahong
Yang, Xianzi
author_sort Li, Zhongwen
collection PubMed
description Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer-related death, especially in China. In addition, the prognosis of late stage patients is extremely poor. However, the biological significance of the long non-coding RNA lnc-ATB and its potential role in ESCC remain to be documented. In this study, we investigated the role of lnc-ATB and the underlying mechanism promoting its oncogenic activity in ESCC. Expression of lnc-ATB was higher in ESCC tissues and cell lines than that in normal counterparts. Upregulated lnc-ATB served as an independent prognosis predictor of ESCC patients. Moreover, loss-of-function assays in ESCC cells showed that knockdown of lnc-ATB inhibited cell proliferation and migration both in vitro and in vivo. Mechanistic investigation indicated that lnc-ATB exerted oncogenic activities via regulating Kindlin-2, as the anti-migration role of lnc-ATB silence was attenuated by ectopic expression of Kindlin-2. Further analysis showed that lnc-ATB functions as a molecular sponge for miR-200b and Kindlin-2. Dysregulated miR-200b/Kindlin-2 signaling mediated the oncogenic activity of lnc-ATB in ESCC. Our results suggest that lnc-ATB predicts poor prognosis and may serve as a potential therapeutic target for ESCC patients.
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spelling pubmed-55209042017-07-27 Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis Li, Zhongwen Wu, Xiaoliang Gu, Ling Shen, Qi Luo, Wen Deng, Chuangzhong Zhou, Qianghua Chen, Xinru Li, Yanjie Lim, ZuanFu Wang, Xing Wang, Jiahong Yang, Xianzi Cell Death Dis Original Article Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer-related death, especially in China. In addition, the prognosis of late stage patients is extremely poor. However, the biological significance of the long non-coding RNA lnc-ATB and its potential role in ESCC remain to be documented. In this study, we investigated the role of lnc-ATB and the underlying mechanism promoting its oncogenic activity in ESCC. Expression of lnc-ATB was higher in ESCC tissues and cell lines than that in normal counterparts. Upregulated lnc-ATB served as an independent prognosis predictor of ESCC patients. Moreover, loss-of-function assays in ESCC cells showed that knockdown of lnc-ATB inhibited cell proliferation and migration both in vitro and in vivo. Mechanistic investigation indicated that lnc-ATB exerted oncogenic activities via regulating Kindlin-2, as the anti-migration role of lnc-ATB silence was attenuated by ectopic expression of Kindlin-2. Further analysis showed that lnc-ATB functions as a molecular sponge for miR-200b and Kindlin-2. Dysregulated miR-200b/Kindlin-2 signaling mediated the oncogenic activity of lnc-ATB in ESCC. Our results suggest that lnc-ATB predicts poor prognosis and may serve as a potential therapeutic target for ESCC patients. Nature Publishing Group 2017-06 2017-06-22 /pmc/articles/PMC5520904/ /pubmed/28640252 http://dx.doi.org/10.1038/cddis.2017.245 Text en Copyright © 2017 The Author(s) http://creativecommons.org/licenses/by/4.0/ Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/
spellingShingle Original Article
Li, Zhongwen
Wu, Xiaoliang
Gu, Ling
Shen, Qi
Luo, Wen
Deng, Chuangzhong
Zhou, Qianghua
Chen, Xinru
Li, Yanjie
Lim, ZuanFu
Wang, Xing
Wang, Jiahong
Yang, Xianzi
Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis
title Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis
title_full Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis
title_fullStr Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis
title_full_unstemmed Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis
title_short Long non-coding RNA ATB promotes malignancy of esophageal squamous cell carcinoma by regulating miR-200b/Kindlin-2 axis
title_sort long non-coding rna atb promotes malignancy of esophageal squamous cell carcinoma by regulating mir-200b/kindlin-2 axis
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5520904/
https://www.ncbi.nlm.nih.gov/pubmed/28640252
http://dx.doi.org/10.1038/cddis.2017.245
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