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MicroRNA-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting VEGFA expression in breast carcinoma

MicroRNAs (miRNAs), a class of small noncoding RNA molecules, can manipulate the expressions of endogenous tumor-related genes, and are implicated in the development and progression of a wide type of tumors. In this study, the investigation from real-time quantitative PCR revealed that miRNA-16-5p w...

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Autores principales: Qu, Yunhui, Liu, Hongtao, Lv, Xinquan, Liu, Yuqiong, Wang, Xiaojuan, Zhang, Min, Zhang, Xiaqing, Li, Yuenan, Lou, Qianqian, Li, Shenglei, Li, Huixiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5641140/
https://www.ncbi.nlm.nih.gov/pubmed/29069797
http://dx.doi.org/10.18632/oncotarget.20398
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author Qu, Yunhui
Liu, Hongtao
Lv, Xinquan
Liu, Yuqiong
Wang, Xiaojuan
Zhang, Min
Zhang, Xiaqing
Li, Yuenan
Lou, Qianqian
Li, Shenglei
Li, Huixiang
author_facet Qu, Yunhui
Liu, Hongtao
Lv, Xinquan
Liu, Yuqiong
Wang, Xiaojuan
Zhang, Min
Zhang, Xiaqing
Li, Yuenan
Lou, Qianqian
Li, Shenglei
Li, Huixiang
author_sort Qu, Yunhui
collection PubMed
description MicroRNAs (miRNAs), a class of small noncoding RNA molecules, can manipulate the expressions of endogenous tumor-related genes, and are implicated in the development and progression of a wide type of tumors. In this study, the investigation from real-time quantitative PCR revealed that miRNA-16-5p was downregulated in breast carcinoma tissues and cells, coupled with the elevations of HIF-α and VEGFA protein expressions, compared with normal tissues. Lentiviral armed with miR-16-5p markedly increased the miR-16-5p levels in MCF-7 and MDA-MB-231 cells, compared to blank and NC groups, and miR-16-5p overexpression significantly inhibited the proliferation and colony formation in MCF-7 and MDA-MB-231 cells. Besides, miR-16-5p upregulation markedly induced apoptosis and reduced invasion ability in MCF-7 and MDA-MB-231 cells. Notably, VEGFA was direct target of miR-16-5p. Stepwise investigation from in vitro and in vivo experiments demonstrated that miR-16-5p overexpression suppressed tumor growth and reduced HIF-α and VEGFA expressions in breast carcinoma cells and nude mice tumor tissues. These findings provide novel insights into molecular mechanism involved in the roles of miR-16-5p in tumor development and progression of breast carcinoma, and thus manipulation of miR-16-5p may be a novel potential therapeutic target for future therapies of the patients with breast carcinoma.
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spelling pubmed-56411402017-10-24 MicroRNA-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting VEGFA expression in breast carcinoma Qu, Yunhui Liu, Hongtao Lv, Xinquan Liu, Yuqiong Wang, Xiaojuan Zhang, Min Zhang, Xiaqing Li, Yuenan Lou, Qianqian Li, Shenglei Li, Huixiang Oncotarget Research Paper MicroRNAs (miRNAs), a class of small noncoding RNA molecules, can manipulate the expressions of endogenous tumor-related genes, and are implicated in the development and progression of a wide type of tumors. In this study, the investigation from real-time quantitative PCR revealed that miRNA-16-5p was downregulated in breast carcinoma tissues and cells, coupled with the elevations of HIF-α and VEGFA protein expressions, compared with normal tissues. Lentiviral armed with miR-16-5p markedly increased the miR-16-5p levels in MCF-7 and MDA-MB-231 cells, compared to blank and NC groups, and miR-16-5p overexpression significantly inhibited the proliferation and colony formation in MCF-7 and MDA-MB-231 cells. Besides, miR-16-5p upregulation markedly induced apoptosis and reduced invasion ability in MCF-7 and MDA-MB-231 cells. Notably, VEGFA was direct target of miR-16-5p. Stepwise investigation from in vitro and in vivo experiments demonstrated that miR-16-5p overexpression suppressed tumor growth and reduced HIF-α and VEGFA expressions in breast carcinoma cells and nude mice tumor tissues. These findings provide novel insights into molecular mechanism involved in the roles of miR-16-5p in tumor development and progression of breast carcinoma, and thus manipulation of miR-16-5p may be a novel potential therapeutic target for future therapies of the patients with breast carcinoma. Impact Journals LLC 2017-08-23 /pmc/articles/PMC5641140/ /pubmed/29069797 http://dx.doi.org/10.18632/oncotarget.20398 Text en Copyright: © 2017 Qu et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Research Paper
Qu, Yunhui
Liu, Hongtao
Lv, Xinquan
Liu, Yuqiong
Wang, Xiaojuan
Zhang, Min
Zhang, Xiaqing
Li, Yuenan
Lou, Qianqian
Li, Shenglei
Li, Huixiang
MicroRNA-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting VEGFA expression in breast carcinoma
title MicroRNA-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting VEGFA expression in breast carcinoma
title_full MicroRNA-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting VEGFA expression in breast carcinoma
title_fullStr MicroRNA-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting VEGFA expression in breast carcinoma
title_full_unstemmed MicroRNA-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting VEGFA expression in breast carcinoma
title_short MicroRNA-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting VEGFA expression in breast carcinoma
title_sort microrna-16-5p overexpression suppresses proliferation and invasion as well as triggers apoptosis by targeting vegfa expression in breast carcinoma
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5641140/
https://www.ncbi.nlm.nih.gov/pubmed/29069797
http://dx.doi.org/10.18632/oncotarget.20398
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