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Downregulation of miR-637 promotes proliferation and metastasis by targeting Smad3 in keloids

Keloids are a type of abnormal scar tissue. MicroRNAs (miRNAs) exhibit a pivotal role in the regulation of cell proliferation and metastasis of keloids. miRNA microarray revealed that miR-637 was one of the most frequently altered miRNAs in keloids. Furthermore, upregulation of miR-637 inhibited cel...

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Detalles Bibliográficos
Autores principales: Zhang, Ye, Guo, Bingyu, Hui, Qiang, Li, Wei, Chang, Peng, Tao, Kai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6072149/
https://www.ncbi.nlm.nih.gov/pubmed/29845237
http://dx.doi.org/10.3892/mmr.2018.9099
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author Zhang, Ye
Guo, Bingyu
Hui, Qiang
Li, Wei
Chang, Peng
Tao, Kai
author_facet Zhang, Ye
Guo, Bingyu
Hui, Qiang
Li, Wei
Chang, Peng
Tao, Kai
author_sort Zhang, Ye
collection PubMed
description Keloids are a type of abnormal scar tissue. MicroRNAs (miRNAs) exhibit a pivotal role in the regulation of cell proliferation and metastasis of keloids. miRNA microarray revealed that miR-637 was one of the most frequently altered miRNAs in keloids. Furthermore, upregulation of miR-637 inhibited cell proliferation and metastasis by targeting mothers against decapentaplegic homolog (Smad)3, one of the important proteins that affects the formation of keloids. Further studies demonstrated that miR-637 regulated the proliferation and metastasis of human keloid fibroblast (HKF) cells by mediating the Smad3 signaling pathway. Overall, the present findings suggest that miR-637 may be a promising therapeutic target in keloids.
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spelling pubmed-60721492018-08-06 Downregulation of miR-637 promotes proliferation and metastasis by targeting Smad3 in keloids Zhang, Ye Guo, Bingyu Hui, Qiang Li, Wei Chang, Peng Tao, Kai Mol Med Rep Articles Keloids are a type of abnormal scar tissue. MicroRNAs (miRNAs) exhibit a pivotal role in the regulation of cell proliferation and metastasis of keloids. miRNA microarray revealed that miR-637 was one of the most frequently altered miRNAs in keloids. Furthermore, upregulation of miR-637 inhibited cell proliferation and metastasis by targeting mothers against decapentaplegic homolog (Smad)3, one of the important proteins that affects the formation of keloids. Further studies demonstrated that miR-637 regulated the proliferation and metastasis of human keloid fibroblast (HKF) cells by mediating the Smad3 signaling pathway. Overall, the present findings suggest that miR-637 may be a promising therapeutic target in keloids. D.A. Spandidos 2018-08 2018-05-29 /pmc/articles/PMC6072149/ /pubmed/29845237 http://dx.doi.org/10.3892/mmr.2018.9099 Text en Copyright: © Zhang et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Zhang, Ye
Guo, Bingyu
Hui, Qiang
Li, Wei
Chang, Peng
Tao, Kai
Downregulation of miR-637 promotes proliferation and metastasis by targeting Smad3 in keloids
title Downregulation of miR-637 promotes proliferation and metastasis by targeting Smad3 in keloids
title_full Downregulation of miR-637 promotes proliferation and metastasis by targeting Smad3 in keloids
title_fullStr Downregulation of miR-637 promotes proliferation and metastasis by targeting Smad3 in keloids
title_full_unstemmed Downregulation of miR-637 promotes proliferation and metastasis by targeting Smad3 in keloids
title_short Downregulation of miR-637 promotes proliferation and metastasis by targeting Smad3 in keloids
title_sort downregulation of mir-637 promotes proliferation and metastasis by targeting smad3 in keloids
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6072149/
https://www.ncbi.nlm.nih.gov/pubmed/29845237
http://dx.doi.org/10.3892/mmr.2018.9099
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