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miR-340 and ZEB1 negative feedback loop regulates TGF-β- mediated breast cancer progression

MicroRNAs act as key regulators in carcinogenesis and progression in various cancers. In present study, we explored the role of miR-340 in the breast cancer progression. Our results showed that overexpression of miR-340 inhibits breast cancer cell proliferation and invasion, whereas depletion of miR...

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Autores principales: Hou, Li-Kun, Yu, Yue, Xie, Ye-Gong, Wang, Jie, Mao, Jie-Fei, Zhang, Bin, Wang, Xin, Cao, Xu-Chen
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5041961/
https://www.ncbi.nlm.nih.gov/pubmed/27036021
http://dx.doi.org/10.18632/oncotarget.8421
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author Hou, Li-Kun
Yu, Yue
Xie, Ye-Gong
Wang, Jie
Mao, Jie-Fei
Zhang, Bin
Wang, Xin
Cao, Xu-Chen
author_facet Hou, Li-Kun
Yu, Yue
Xie, Ye-Gong
Wang, Jie
Mao, Jie-Fei
Zhang, Bin
Wang, Xin
Cao, Xu-Chen
author_sort Hou, Li-Kun
collection PubMed
description MicroRNAs act as key regulators in carcinogenesis and progression in various cancers. In present study, we explored the role of miR-340 in the breast cancer progression. Our results showed that overexpression of miR-340 inhibits breast cancer cell proliferation and invasion, whereas depletion of miR-340 promotes breast cancer progression. Molecularly, ZEB1 was identified as a target gene of miR-340 and miR-340 suppressed the expression of ZEB1 by directly binding to the 3′-UTR of ZEB1. Furthermore, ZEB1 transcriptionally suppresses miR-340 expression. The negative feedback loop regulated TGF-β-mediated breast cancer progression. In conclusion, our data suggested that miR-340 acted as a tumor suppressor in breast cancer progression.
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spelling pubmed-50419612016-10-10 miR-340 and ZEB1 negative feedback loop regulates TGF-β- mediated breast cancer progression Hou, Li-Kun Yu, Yue Xie, Ye-Gong Wang, Jie Mao, Jie-Fei Zhang, Bin Wang, Xin Cao, Xu-Chen Oncotarget Research Paper MicroRNAs act as key regulators in carcinogenesis and progression in various cancers. In present study, we explored the role of miR-340 in the breast cancer progression. Our results showed that overexpression of miR-340 inhibits breast cancer cell proliferation and invasion, whereas depletion of miR-340 promotes breast cancer progression. Molecularly, ZEB1 was identified as a target gene of miR-340 and miR-340 suppressed the expression of ZEB1 by directly binding to the 3′-UTR of ZEB1. Furthermore, ZEB1 transcriptionally suppresses miR-340 expression. The negative feedback loop regulated TGF-β-mediated breast cancer progression. In conclusion, our data suggested that miR-340 acted as a tumor suppressor in breast cancer progression. Impact Journals LLC 2016-03-27 /pmc/articles/PMC5041961/ /pubmed/27036021 http://dx.doi.org/10.18632/oncotarget.8421 Text en Copyright: © 2016 Hou 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
Hou, Li-Kun
Yu, Yue
Xie, Ye-Gong
Wang, Jie
Mao, Jie-Fei
Zhang, Bin
Wang, Xin
Cao, Xu-Chen
miR-340 and ZEB1 negative feedback loop regulates TGF-β- mediated breast cancer progression
title miR-340 and ZEB1 negative feedback loop regulates TGF-β- mediated breast cancer progression
title_full miR-340 and ZEB1 negative feedback loop regulates TGF-β- mediated breast cancer progression
title_fullStr miR-340 and ZEB1 negative feedback loop regulates TGF-β- mediated breast cancer progression
title_full_unstemmed miR-340 and ZEB1 negative feedback loop regulates TGF-β- mediated breast cancer progression
title_short miR-340 and ZEB1 negative feedback loop regulates TGF-β- mediated breast cancer progression
title_sort mir-340 and zeb1 negative feedback loop regulates tgf-β- mediated breast cancer progression
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5041961/
https://www.ncbi.nlm.nih.gov/pubmed/27036021
http://dx.doi.org/10.18632/oncotarget.8421
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