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Mir-338-3p Inhibits Malignant Biological Behaviors of Glioma Cells by Targeting MACC1 Gene

BACKGROUND: Human brain glioma is the most common endocranial tumor; its mortality and morbidity are very high. The objective of this study was to determine whether miR-338-3p can regulate malignant biological behaviors of glioma cells by targeted silencing of MACC1. MATERIAL/METHODS: The expression...

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Autores principales: Shang, Chao, Hong, Yang, Guo, Yan, Xue, Yi-xue
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4780270/
https://www.ncbi.nlm.nih.gov/pubmed/26936749
http://dx.doi.org/10.12659/MSM.897055
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author Shang, Chao
Hong, Yang
Guo, Yan
Xue, Yi-xue
author_facet Shang, Chao
Hong, Yang
Guo, Yan
Xue, Yi-xue
author_sort Shang, Chao
collection PubMed
description BACKGROUND: Human brain glioma is the most common endocranial tumor; its mortality and morbidity are very high. The objective of this study was to determine whether miR-338-3p can regulate malignant biological behaviors of glioma cells by targeted silencing of MACC1. MATERIAL/METHODS: The expression of miR-338-3p was detected by quantitative real-time PCR in brain glioma tissues and cell lines. Bioinformatics software was used to predict some potential target genes of miR-338-3p. Luciferase activities assay was used to verify the combination between target genes and miR-338-3p. And MACC1 protein expression was detected by Western blot. The apoptosis and proliferation ability were analyzed by MTT and flow cytometry assay. RESULTS: Compared with normal brain tissues and cells, miR-338-3p in glioma tissues and cell lines was confirmed to be expressed at low levels, and down-regulation of miR-338-3p tended to be correlated with worse histological grade. Up-regulation of miR-338-3p promoted apoptosis and sharply inhibited cell proliferation ability of U251 and U87 cells. The luciferase activities assay, biotin-avidin pull-down assay, and western blot analysis verified that MACC1 was a specific target gene of miR-338-3p. Subsequent experiments found that up-regulation of MACC1 significantly inhibited the apoptosis and increased the cell proliferation ability of U251 and U87 cells. The regulation effects of miR-338-3p on malignant biological behaviors of glioma cells can be partly reversed by up-regulation of MACC1. CONCLUSIONS: Down-regulation of miR-338-3p was an independent prognostic biomarker associated with poor prognosis in glioma patients; miR-338-3p acted as a tumor-suppressing gene whose silencing can inhibit malignant biological behaviors of glioma cells. MACC1 was a specific target gene of miR-338-3p, which regulates malignant biological behaviors of glioma cells partly through directly silencing MACC1 expression.
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spelling pubmed-47802702016-03-18 Mir-338-3p Inhibits Malignant Biological Behaviors of Glioma Cells by Targeting MACC1 Gene Shang, Chao Hong, Yang Guo, Yan Xue, Yi-xue Med Sci Monit Lab/In Vitro Research BACKGROUND: Human brain glioma is the most common endocranial tumor; its mortality and morbidity are very high. The objective of this study was to determine whether miR-338-3p can regulate malignant biological behaviors of glioma cells by targeted silencing of MACC1. MATERIAL/METHODS: The expression of miR-338-3p was detected by quantitative real-time PCR in brain glioma tissues and cell lines. Bioinformatics software was used to predict some potential target genes of miR-338-3p. Luciferase activities assay was used to verify the combination between target genes and miR-338-3p. And MACC1 protein expression was detected by Western blot. The apoptosis and proliferation ability were analyzed by MTT and flow cytometry assay. RESULTS: Compared with normal brain tissues and cells, miR-338-3p in glioma tissues and cell lines was confirmed to be expressed at low levels, and down-regulation of miR-338-3p tended to be correlated with worse histological grade. Up-regulation of miR-338-3p promoted apoptosis and sharply inhibited cell proliferation ability of U251 and U87 cells. The luciferase activities assay, biotin-avidin pull-down assay, and western blot analysis verified that MACC1 was a specific target gene of miR-338-3p. Subsequent experiments found that up-regulation of MACC1 significantly inhibited the apoptosis and increased the cell proliferation ability of U251 and U87 cells. The regulation effects of miR-338-3p on malignant biological behaviors of glioma cells can be partly reversed by up-regulation of MACC1. CONCLUSIONS: Down-regulation of miR-338-3p was an independent prognostic biomarker associated with poor prognosis in glioma patients; miR-338-3p acted as a tumor-suppressing gene whose silencing can inhibit malignant biological behaviors of glioma cells. MACC1 was a specific target gene of miR-338-3p, which regulates malignant biological behaviors of glioma cells partly through directly silencing MACC1 expression. International Scientific Literature, Inc. 2016-03-03 /pmc/articles/PMC4780270/ /pubmed/26936749 http://dx.doi.org/10.12659/MSM.897055 Text en © Med Sci Monit, 2016 This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License
spellingShingle Lab/In Vitro Research
Shang, Chao
Hong, Yang
Guo, Yan
Xue, Yi-xue
Mir-338-3p Inhibits Malignant Biological Behaviors of Glioma Cells by Targeting MACC1 Gene
title Mir-338-3p Inhibits Malignant Biological Behaviors of Glioma Cells by Targeting MACC1 Gene
title_full Mir-338-3p Inhibits Malignant Biological Behaviors of Glioma Cells by Targeting MACC1 Gene
title_fullStr Mir-338-3p Inhibits Malignant Biological Behaviors of Glioma Cells by Targeting MACC1 Gene
title_full_unstemmed Mir-338-3p Inhibits Malignant Biological Behaviors of Glioma Cells by Targeting MACC1 Gene
title_short Mir-338-3p Inhibits Malignant Biological Behaviors of Glioma Cells by Targeting MACC1 Gene
title_sort mir-338-3p inhibits malignant biological behaviors of glioma cells by targeting macc1 gene
topic Lab/In Vitro Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4780270/
https://www.ncbi.nlm.nih.gov/pubmed/26936749
http://dx.doi.org/10.12659/MSM.897055
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