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miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro
BACKGROUND: MicroRNAs are significantly involved in tumorigenesis and progression of glioma. However, the critical part they play in glioma have not been fully elaborated. miR-491 and Tripartite motif containing 28 (TRIM28) are reported to aberrantly express in glioblastoma multiforme (GBM). Here, w...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5131408/ https://www.ncbi.nlm.nih.gov/pubmed/27905892 http://dx.doi.org/10.1186/s12883-016-0769-y |
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author | Qi, Zengxin Cai, Shengyong Cai, Jiajun Chen, Lingchao Yao, Yu Chen, Liang Mao, Ying |
author_facet | Qi, Zengxin Cai, Shengyong Cai, Jiajun Chen, Lingchao Yao, Yu Chen, Liang Mao, Ying |
author_sort | Qi, Zengxin |
collection | PubMed |
description | BACKGROUND: MicroRNAs are significantly involved in tumorigenesis and progression of glioma. However, the critical part they play in glioma have not been fully elaborated. miR-491 and Tripartite motif containing 28 (TRIM28) are reported to aberrantly express in glioblastoma multiforme (GBM). Here, we detected miR-491 and TRIM28 expression and function in glioma cells. METHODS: We analyzed miR-491 expressions in 20 primary human GBM tissues and 6 control brain tissues by qRT-PCR assays and searched for The Cancer Genome Atlas (TCGA) database. Then we predicted possible mRNA target of miR-491 by TargetScan/MicroRNA and confirmed it via luciferase reporter assays. Knock-down of miR-491 and transfection of pLenti-TRIM28 were performed in U251 and U87 cells. Proliferation ability was examined by MTT and clone formation assays. RESULTS: miR-491 expression was obviously reduced in GBM cells and tissues. There was a positive correlation between the down-regulation of miR-491 and poor prognosis. Spearman’s correlation analysis demonstrated that miR-491 expression was negatively correlated with TRIM28 protein level. Possible mRNA binding sites of miR-491 predicted by TargetScan/MicroRNA were proved by luciferase assays. Clone formation and MTT assays indicated that up-regulation of miR-491 inhibited the proliferation of glioma cells. CONCLUSIONS: miR-491 regulates glioma cells proliferation in vitro by targeting TRIM28. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12883-016-0769-y) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-5131408 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-51314082016-12-12 miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro Qi, Zengxin Cai, Shengyong Cai, Jiajun Chen, Lingchao Yao, Yu Chen, Liang Mao, Ying BMC Neurol Research Article BACKGROUND: MicroRNAs are significantly involved in tumorigenesis and progression of glioma. However, the critical part they play in glioma have not been fully elaborated. miR-491 and Tripartite motif containing 28 (TRIM28) are reported to aberrantly express in glioblastoma multiforme (GBM). Here, we detected miR-491 and TRIM28 expression and function in glioma cells. METHODS: We analyzed miR-491 expressions in 20 primary human GBM tissues and 6 control brain tissues by qRT-PCR assays and searched for The Cancer Genome Atlas (TCGA) database. Then we predicted possible mRNA target of miR-491 by TargetScan/MicroRNA and confirmed it via luciferase reporter assays. Knock-down of miR-491 and transfection of pLenti-TRIM28 were performed in U251 and U87 cells. Proliferation ability was examined by MTT and clone formation assays. RESULTS: miR-491 expression was obviously reduced in GBM cells and tissues. There was a positive correlation between the down-regulation of miR-491 and poor prognosis. Spearman’s correlation analysis demonstrated that miR-491 expression was negatively correlated with TRIM28 protein level. Possible mRNA binding sites of miR-491 predicted by TargetScan/MicroRNA were proved by luciferase assays. Clone formation and MTT assays indicated that up-regulation of miR-491 inhibited the proliferation of glioma cells. CONCLUSIONS: miR-491 regulates glioma cells proliferation in vitro by targeting TRIM28. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12883-016-0769-y) contains supplementary material, which is available to authorized users. BioMed Central 2016-12-01 /pmc/articles/PMC5131408/ /pubmed/27905892 http://dx.doi.org/10.1186/s12883-016-0769-y Text en © The Author(s). 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Article Qi, Zengxin Cai, Shengyong Cai, Jiajun Chen, Lingchao Yao, Yu Chen, Liang Mao, Ying miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro |
title | miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro |
title_full | miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro |
title_fullStr | miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro |
title_full_unstemmed | miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro |
title_short | miR-491 regulates glioma cells proliferation by targeting TRIM28 in vitro |
title_sort | mir-491 regulates glioma cells proliferation by targeting trim28 in vitro |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5131408/ https://www.ncbi.nlm.nih.gov/pubmed/27905892 http://dx.doi.org/10.1186/s12883-016-0769-y |
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