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MiR-210 Up-Regulation Inhibits Proliferation and Induces Apoptosis in Glioma Cells by Targeting SIN3A
BACKGROUND: The aim of this study was to determine whether miR-210 can affect the apoptosis and proliferation of human U251 glioma cells from down-regulating SIN3A. MATERIAL/METHODS: The expression of miRNA-210 was detected by quantitative real-time PCR in normal brain tissue and glioma samples. The...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
International Scientific Literature, Inc.
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266365/ https://www.ncbi.nlm.nih.gov/pubmed/25481483 http://dx.doi.org/10.12659/MSM.892994 |
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author | Shang, Chao Hong, Yang Guo, Yan Liu, Yun-hui Xue, Yi-xue |
author_facet | Shang, Chao Hong, Yang Guo, Yan Liu, Yun-hui Xue, Yi-xue |
author_sort | Shang, Chao |
collection | PubMed |
description | BACKGROUND: The aim of this study was to determine whether miR-210 can affect the apoptosis and proliferation of human U251 glioma cells from down-regulating SIN3A. MATERIAL/METHODS: The expression of miRNA-210 was detected by quantitative real-time PCR in normal brain tissue and glioma samples. The apoptosis and proliferation ability of U251 cells were analyzed by MTT and flow cytometry assay after anti-miR-210 transfection. For the regulation mechanism analysis of miR-210, TargetScan, PicTar, and microRNA were selected to predict some potential target genes of miR-210. The predicted gene was identified to be the direct and specific target gene of miR-210 by luciferase activities assay and Western blot. RNA interference technology was used to confirm that the apoptosis and proliferation effects of miR-210 were directly induced by SIN3A. RESULTS: The expression of miR-210 increased significantly in glioma in comparison with normal brain tissue. The silence of miR-210 expression could inhibit the proliferation of U251 cells and induce the apoptosis. Mechanism analysis revealed that SIN3A was a specific and direct target gene of miR-210. The siRNA-SIN3A could down-regulate the expression of SIN3A protein, which was up-regulated in U251 cells by anti-miR-210 transfection, and our experiments found that silence of SIN3A could inhibit the apoptosis and sharply increase the proliferation of U251 cells. The regulation effects of anti-miR-210 on apoptosis and proliferation can be reversed respectively by the expression silence of SIN3A. CONCLUSIONS: Aberrantly expressed miR-210 regulates human U251 glioma cells apoptosis and proliferation partly through directly down-regulating SIN3A protein expression. This might offer a new potential therapeutic stratagem for glioma. |
format | Online Article Text |
id | pubmed-4266365 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | International Scientific Literature, Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-42663652014-12-16 MiR-210 Up-Regulation Inhibits Proliferation and Induces Apoptosis in Glioma Cells by Targeting SIN3A Shang, Chao Hong, Yang Guo, Yan Liu, Yun-hui Xue, Yi-xue Med Sci Monit Molecular Biology BACKGROUND: The aim of this study was to determine whether miR-210 can affect the apoptosis and proliferation of human U251 glioma cells from down-regulating SIN3A. MATERIAL/METHODS: The expression of miRNA-210 was detected by quantitative real-time PCR in normal brain tissue and glioma samples. The apoptosis and proliferation ability of U251 cells were analyzed by MTT and flow cytometry assay after anti-miR-210 transfection. For the regulation mechanism analysis of miR-210, TargetScan, PicTar, and microRNA were selected to predict some potential target genes of miR-210. The predicted gene was identified to be the direct and specific target gene of miR-210 by luciferase activities assay and Western blot. RNA interference technology was used to confirm that the apoptosis and proliferation effects of miR-210 were directly induced by SIN3A. RESULTS: The expression of miR-210 increased significantly in glioma in comparison with normal brain tissue. The silence of miR-210 expression could inhibit the proliferation of U251 cells and induce the apoptosis. Mechanism analysis revealed that SIN3A was a specific and direct target gene of miR-210. The siRNA-SIN3A could down-regulate the expression of SIN3A protein, which was up-regulated in U251 cells by anti-miR-210 transfection, and our experiments found that silence of SIN3A could inhibit the apoptosis and sharply increase the proliferation of U251 cells. The regulation effects of anti-miR-210 on apoptosis and proliferation can be reversed respectively by the expression silence of SIN3A. CONCLUSIONS: Aberrantly expressed miR-210 regulates human U251 glioma cells apoptosis and proliferation partly through directly down-regulating SIN3A protein expression. This might offer a new potential therapeutic stratagem for glioma. International Scientific Literature, Inc. 2014-12-07 /pmc/articles/PMC4266365/ /pubmed/25481483 http://dx.doi.org/10.12659/MSM.892994 Text en © Med Sci Monit, 2014 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License |
spellingShingle | Molecular Biology Shang, Chao Hong, Yang Guo, Yan Liu, Yun-hui Xue, Yi-xue MiR-210 Up-Regulation Inhibits Proliferation and Induces Apoptosis in Glioma Cells by Targeting SIN3A |
title | MiR-210 Up-Regulation Inhibits Proliferation and Induces Apoptosis in Glioma Cells by Targeting SIN3A |
title_full | MiR-210 Up-Regulation Inhibits Proliferation and Induces Apoptosis in Glioma Cells by Targeting SIN3A |
title_fullStr | MiR-210 Up-Regulation Inhibits Proliferation and Induces Apoptosis in Glioma Cells by Targeting SIN3A |
title_full_unstemmed | MiR-210 Up-Regulation Inhibits Proliferation and Induces Apoptosis in Glioma Cells by Targeting SIN3A |
title_short | MiR-210 Up-Regulation Inhibits Proliferation and Induces Apoptosis in Glioma Cells by Targeting SIN3A |
title_sort | mir-210 up-regulation inhibits proliferation and induces apoptosis in glioma cells by targeting sin3a |
topic | Molecular Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4266365/ https://www.ncbi.nlm.nih.gov/pubmed/25481483 http://dx.doi.org/10.12659/MSM.892994 |
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