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Novel miR-29b target regulation patterns are revealed in two different cell lines
MicroRNAs (miRNAs) are a class of small non-coding RNAs that regulate gene or protein expression by targeting mRNAs and triggering either translational repression or mRNA degradation. Distinct expression levels of miRNAs, including miR-29b, have been detected in various biological fluids and tissues...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6877611/ https://www.ncbi.nlm.nih.gov/pubmed/31767948 http://dx.doi.org/10.1038/s41598-019-53868-x |
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author | Zhao, Wenting Cheng, Lesley Quek, Camelia Bellingham, Shayne A. Hill, Andrew F. |
author_facet | Zhao, Wenting Cheng, Lesley Quek, Camelia Bellingham, Shayne A. Hill, Andrew F. |
author_sort | Zhao, Wenting |
collection | PubMed |
description | MicroRNAs (miRNAs) are a class of small non-coding RNAs that regulate gene or protein expression by targeting mRNAs and triggering either translational repression or mRNA degradation. Distinct expression levels of miRNAs, including miR-29b, have been detected in various biological fluids and tissues from a large variety of disease models. However, how miRNAs “react” and function in different cellular environments is still largely unknown. In this study, the regulation patterns of miR-29b between human and mouse cell lines were compared for the first time. CRISPR/Cas9 gene editing was used to stably knockdown miR-29b in human cancer HeLa cells and mouse fibroblast NIH/3T3 cells with minimum off-targets. Genome editing revealed mir-29b-1, other than mir-29b-2, to be the main source of generating mature miR-29b. The editing of miR-29b decreased expression levels of its family members miR-29a/c via changing the tertiary structures of surrounding nucleotides. Comparing transcriptome profiles of human and mouse cell lines, miR-29b displayed common regulation pathways involving distinct downstream targets in macromolecular complex assembly, cell cycle regulation, and Wnt and PI3K-Akt signalling pathways; miR-29b also demonstrated specific functions reflecting cell characteristics, including fibrosis and neuronal regulations in NIH/3T3 cells and tumorigenesis and cellular senescence in HeLa cells. |
format | Online Article Text |
id | pubmed-6877611 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-68776112019-12-05 Novel miR-29b target regulation patterns are revealed in two different cell lines Zhao, Wenting Cheng, Lesley Quek, Camelia Bellingham, Shayne A. Hill, Andrew F. Sci Rep Article MicroRNAs (miRNAs) are a class of small non-coding RNAs that regulate gene or protein expression by targeting mRNAs and triggering either translational repression or mRNA degradation. Distinct expression levels of miRNAs, including miR-29b, have been detected in various biological fluids and tissues from a large variety of disease models. However, how miRNAs “react” and function in different cellular environments is still largely unknown. In this study, the regulation patterns of miR-29b between human and mouse cell lines were compared for the first time. CRISPR/Cas9 gene editing was used to stably knockdown miR-29b in human cancer HeLa cells and mouse fibroblast NIH/3T3 cells with minimum off-targets. Genome editing revealed mir-29b-1, other than mir-29b-2, to be the main source of generating mature miR-29b. The editing of miR-29b decreased expression levels of its family members miR-29a/c via changing the tertiary structures of surrounding nucleotides. Comparing transcriptome profiles of human and mouse cell lines, miR-29b displayed common regulation pathways involving distinct downstream targets in macromolecular complex assembly, cell cycle regulation, and Wnt and PI3K-Akt signalling pathways; miR-29b also demonstrated specific functions reflecting cell characteristics, including fibrosis and neuronal regulations in NIH/3T3 cells and tumorigenesis and cellular senescence in HeLa cells. Nature Publishing Group UK 2019-11-25 /pmc/articles/PMC6877611/ /pubmed/31767948 http://dx.doi.org/10.1038/s41598-019-53868-x Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Zhao, Wenting Cheng, Lesley Quek, Camelia Bellingham, Shayne A. Hill, Andrew F. Novel miR-29b target regulation patterns are revealed in two different cell lines |
title | Novel miR-29b target regulation patterns are revealed in two different cell lines |
title_full | Novel miR-29b target regulation patterns are revealed in two different cell lines |
title_fullStr | Novel miR-29b target regulation patterns are revealed in two different cell lines |
title_full_unstemmed | Novel miR-29b target regulation patterns are revealed in two different cell lines |
title_short | Novel miR-29b target regulation patterns are revealed in two different cell lines |
title_sort | novel mir-29b target regulation patterns are revealed in two different cell lines |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6877611/ https://www.ncbi.nlm.nih.gov/pubmed/31767948 http://dx.doi.org/10.1038/s41598-019-53868-x |
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