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MiR-18a regulates myoblasts proliferation by targeting Fgf1

MiRNAs play an important role in cell proliferation, apoptosis, and differentiation. MiR-18a is increasingly being recognized as a regulator of cancer pathogenesis. Here, we discovered that miR-18a participates in myoblasts proliferation. Expression of miR-18a was downregulated with the differentiat...

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Detalles Bibliográficos
Autores principales: Liu, Chuncheng, Chen, Min, Wang, Meng, Pi, Wenhui, Li, Ning, Meng, Qingyong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6067758/
https://www.ncbi.nlm.nih.gov/pubmed/30063763
http://dx.doi.org/10.1371/journal.pone.0201551
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author Liu, Chuncheng
Chen, Min
Wang, Meng
Pi, Wenhui
Li, Ning
Meng, Qingyong
author_facet Liu, Chuncheng
Chen, Min
Wang, Meng
Pi, Wenhui
Li, Ning
Meng, Qingyong
author_sort Liu, Chuncheng
collection PubMed
description MiRNAs play an important role in cell proliferation, apoptosis, and differentiation. MiR-18a is increasingly being recognized as a regulator of cancer pathogenesis. Here, we discovered that miR-18a participates in myoblasts proliferation. Expression of miR-18a was downregulated with the differentiation of C2C12 myoblasts. Overexpression of miR-18a affected the proliferation of C2C12 cells, primary myoblasts and RD cells. MiR-18a influenced the expression of cell cycle-related genes. Using TargetScan 6.2, we found that the 3’ untranslated region (UTR) of the mouse Fgf1 gene contains complementary sequences to miR-18a. Using a siRNA, we confirmed that the reduction in the Fgf1 levels inhibited proliferation of C2C12 cells. Therefore, our results show that miR-18a participates in the regulation of proliferation by partly decreasing the expression of Fgf1.
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spelling pubmed-60677582018-08-10 MiR-18a regulates myoblasts proliferation by targeting Fgf1 Liu, Chuncheng Chen, Min Wang, Meng Pi, Wenhui Li, Ning Meng, Qingyong PLoS One Research Article MiRNAs play an important role in cell proliferation, apoptosis, and differentiation. MiR-18a is increasingly being recognized as a regulator of cancer pathogenesis. Here, we discovered that miR-18a participates in myoblasts proliferation. Expression of miR-18a was downregulated with the differentiation of C2C12 myoblasts. Overexpression of miR-18a affected the proliferation of C2C12 cells, primary myoblasts and RD cells. MiR-18a influenced the expression of cell cycle-related genes. Using TargetScan 6.2, we found that the 3’ untranslated region (UTR) of the mouse Fgf1 gene contains complementary sequences to miR-18a. Using a siRNA, we confirmed that the reduction in the Fgf1 levels inhibited proliferation of C2C12 cells. Therefore, our results show that miR-18a participates in the regulation of proliferation by partly decreasing the expression of Fgf1. Public Library of Science 2018-07-31 /pmc/articles/PMC6067758/ /pubmed/30063763 http://dx.doi.org/10.1371/journal.pone.0201551 Text en © 2018 Liu 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 (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Liu, Chuncheng
Chen, Min
Wang, Meng
Pi, Wenhui
Li, Ning
Meng, Qingyong
MiR-18a regulates myoblasts proliferation by targeting Fgf1
title MiR-18a regulates myoblasts proliferation by targeting Fgf1
title_full MiR-18a regulates myoblasts proliferation by targeting Fgf1
title_fullStr MiR-18a regulates myoblasts proliferation by targeting Fgf1
title_full_unstemmed MiR-18a regulates myoblasts proliferation by targeting Fgf1
title_short MiR-18a regulates myoblasts proliferation by targeting Fgf1
title_sort mir-18a regulates myoblasts proliferation by targeting fgf1
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6067758/
https://www.ncbi.nlm.nih.gov/pubmed/30063763
http://dx.doi.org/10.1371/journal.pone.0201551
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