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miR-506 Regulates Epithelial Mesenchymal Transition in Breast Cancer Cell Lines
Epithelial-mesenchymal transition (EMT) is an important parameter related to breast cancer survival. Among several microRNAs predicted to target EMT-related genes, miR-506 is a novel miRNA found to be significantly related to breast cancer patient survival in a meta-analysis. miR-506 suppressed the...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3661463/ https://www.ncbi.nlm.nih.gov/pubmed/23717581 http://dx.doi.org/10.1371/journal.pone.0064273 |
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author | Arora, Himanshu Qureshi, Rehana Park, Woong-Yang |
author_facet | Arora, Himanshu Qureshi, Rehana Park, Woong-Yang |
author_sort | Arora, Himanshu |
collection | PubMed |
description | Epithelial-mesenchymal transition (EMT) is an important parameter related to breast cancer survival. Among several microRNAs predicted to target EMT-related genes, miR-506 is a novel miRNA found to be significantly related to breast cancer patient survival in a meta-analysis. miR-506 suppressed the expression of mesenchymal genes such as Vimentin, Snai2, and CD151 in MDA-MB-231 human breast cancer cell line. Moreover, NF-κB bound to the upstream promoter region of miR-506 to suppress transcription. Overexpression of miR-506 inhibited TGFβ-induced EMT and suppressed adhesion, invasion, and migration of MDA-MB-231 cells. From these results, we concluded that miR-506 plays a key role in the process of EMT through posttranslational control of EMT-related genes. |
format | Online Article Text |
id | pubmed-3661463 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-36614632013-05-28 miR-506 Regulates Epithelial Mesenchymal Transition in Breast Cancer Cell Lines Arora, Himanshu Qureshi, Rehana Park, Woong-Yang PLoS One Research Article Epithelial-mesenchymal transition (EMT) is an important parameter related to breast cancer survival. Among several microRNAs predicted to target EMT-related genes, miR-506 is a novel miRNA found to be significantly related to breast cancer patient survival in a meta-analysis. miR-506 suppressed the expression of mesenchymal genes such as Vimentin, Snai2, and CD151 in MDA-MB-231 human breast cancer cell line. Moreover, NF-κB bound to the upstream promoter region of miR-506 to suppress transcription. Overexpression of miR-506 inhibited TGFβ-induced EMT and suppressed adhesion, invasion, and migration of MDA-MB-231 cells. From these results, we concluded that miR-506 plays a key role in the process of EMT through posttranslational control of EMT-related genes. Public Library of Science 2013-05-22 /pmc/articles/PMC3661463/ /pubmed/23717581 http://dx.doi.org/10.1371/journal.pone.0064273 Text en © 2013 Arora et al http://creativecommons.org/licenses/by/4.0/ 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 properly credited. |
spellingShingle | Research Article Arora, Himanshu Qureshi, Rehana Park, Woong-Yang miR-506 Regulates Epithelial Mesenchymal Transition in Breast Cancer Cell Lines |
title | miR-506 Regulates Epithelial Mesenchymal Transition in Breast Cancer Cell Lines |
title_full | miR-506 Regulates Epithelial Mesenchymal Transition in Breast Cancer Cell Lines |
title_fullStr | miR-506 Regulates Epithelial Mesenchymal Transition in Breast Cancer Cell Lines |
title_full_unstemmed | miR-506 Regulates Epithelial Mesenchymal Transition in Breast Cancer Cell Lines |
title_short | miR-506 Regulates Epithelial Mesenchymal Transition in Breast Cancer Cell Lines |
title_sort | mir-506 regulates epithelial mesenchymal transition in breast cancer cell lines |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3661463/ https://www.ncbi.nlm.nih.gov/pubmed/23717581 http://dx.doi.org/10.1371/journal.pone.0064273 |
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