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LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

Pancreatic cancer is one of the most deadly cancers with a poor prognosis. Though studies have implicated the roles of microRNAs in pancreatic cancer progression, little is known about the role of miR-613 in pancreatic cancer. In the present study, the expression of miR-613 was down-regulated in pan...

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Autores principales: Cai, Huihua, Yao, Jie, An, Yong, Chen, Xuemin, Chen, Weibo, Wu, Di, Luo, Boyang, Yang, Yong, Jiang, Yong, Sun, Donglin, He, Xiaozhou
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5464837/
https://www.ncbi.nlm.nih.gov/pubmed/28415631
http://dx.doi.org/10.18632/oncotarget.16462
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author Cai, Huihua
Yao, Jie
An, Yong
Chen, Xuemin
Chen, Weibo
Wu, Di
Luo, Boyang
Yang, Yong
Jiang, Yong
Sun, Donglin
He, Xiaozhou
author_facet Cai, Huihua
Yao, Jie
An, Yong
Chen, Xuemin
Chen, Weibo
Wu, Di
Luo, Boyang
Yang, Yong
Jiang, Yong
Sun, Donglin
He, Xiaozhou
author_sort Cai, Huihua
collection PubMed
description Pancreatic cancer is one of the most deadly cancers with a poor prognosis. Though studies have implicated the roles of microRNAs in pancreatic cancer progression, little is known about the role of miR-613 in pancreatic cancer. In the present study, the expression of miR-613 was down-regulated in pancreatic cancer tissues and cancer cell lines. Down-regulation of miR-613 was positively correlated with tumor differentiation, advanced TNM stage, nodal metastasis and shorter overall survival in patients with pancreatic cancer. Overexpression of miR-613 suppressed cell proliferation, invasion and migration, and induced cell apoptosis and cell cycle arrest at G0/G1 phase in pancreatic cancer cells. Bioinformatics analysis, luciferase reporter assay and rescue experiments showed that notch3 was a direct target of miR-613. MiR-613 was inversely correlated with notch3 expression in pancreatic cancer tissues. The long non-coding RNA, HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines, and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA. In vivo studies showed that stable overexpression of miR-613 or knock-down of HOTAIR suppressed tumor growth and also reduced the expression of notch3. In conclusion, these results suggest that HOTAIR functions as a competing endogenous RNA to regulate notch3 expression via sponging miR-613 in pancreatic cancer.
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spelling pubmed-54648372017-06-21 LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer Cai, Huihua Yao, Jie An, Yong Chen, Xuemin Chen, Weibo Wu, Di Luo, Boyang Yang, Yong Jiang, Yong Sun, Donglin He, Xiaozhou Oncotarget Research Paper Pancreatic cancer is one of the most deadly cancers with a poor prognosis. Though studies have implicated the roles of microRNAs in pancreatic cancer progression, little is known about the role of miR-613 in pancreatic cancer. In the present study, the expression of miR-613 was down-regulated in pancreatic cancer tissues and cancer cell lines. Down-regulation of miR-613 was positively correlated with tumor differentiation, advanced TNM stage, nodal metastasis and shorter overall survival in patients with pancreatic cancer. Overexpression of miR-613 suppressed cell proliferation, invasion and migration, and induced cell apoptosis and cell cycle arrest at G0/G1 phase in pancreatic cancer cells. Bioinformatics analysis, luciferase reporter assay and rescue experiments showed that notch3 was a direct target of miR-613. MiR-613 was inversely correlated with notch3 expression in pancreatic cancer tissues. The long non-coding RNA, HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines, and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA. In vivo studies showed that stable overexpression of miR-613 or knock-down of HOTAIR suppressed tumor growth and also reduced the expression of notch3. In conclusion, these results suggest that HOTAIR functions as a competing endogenous RNA to regulate notch3 expression via sponging miR-613 in pancreatic cancer. Impact Journals LLC 2017-03-22 /pmc/articles/PMC5464837/ /pubmed/28415631 http://dx.doi.org/10.18632/oncotarget.16462 Text en Copyright: © 2017 Cai 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
Cai, Huihua
Yao, Jie
An, Yong
Chen, Xuemin
Chen, Weibo
Wu, Di
Luo, Boyang
Yang, Yong
Jiang, Yong
Sun, Donglin
He, Xiaozhou
LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer
title LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer
title_full LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer
title_fullStr LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer
title_full_unstemmed LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer
title_short LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer
title_sort lncrna hotair acts as competing endogenous rna to control the expression of notch3 via sponging mir-613 in pancreatic cancer
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5464837/
https://www.ncbi.nlm.nih.gov/pubmed/28415631
http://dx.doi.org/10.18632/oncotarget.16462
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