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miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling
Objective: Micro-RNA plays a critical role in the pathological process of gliomas. Previous research showed that the level of miR-155 was significantly increased in many cancers, including gliomas. However, the mechanism of glioma is still unknown. Method: To investigate the regulatory function of m...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2020
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7198892/ https://www.ncbi.nlm.nih.gov/pubmed/32411077 http://dx.doi.org/10.3389/fneur.2020.00297 |
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author | Wu, Dahao Wang, Changzhen |
author_facet | Wu, Dahao Wang, Changzhen |
author_sort | Wu, Dahao |
collection | PubMed |
description | Objective: Micro-RNA plays a critical role in the pathological process of gliomas. Previous research showed that the level of miR-155 was significantly increased in many cancers, including gliomas. However, the mechanism of glioma is still unknown. Method: To investigate the regulatory function of miR-155 on glioma U87-MG cells and its effects on related signaling pathways. After transfection of miR-155 mimic and inhibitor, the level of miR-155 were applied to detect cell proliferation, apoptosis, senescence index, invasive ability and cell migration at different time points (0, 24, 24 h, respectively) by CCK8 assay, flow cytometry, β-galactosidase (β-gal) staining, transwell and scratch test, respectively. The effect of miR-155 on PI3K/AKT signal pathway was observed at meantime. Results: Compared with the control group, after miR-155 mimic transfection, U87-MG cell viability, cell migration rate and invasiveness were increased, while apoptosis and senescence were significantly decreased, which was the opposite on miR-155 inhibitor transfection. The phosphorylation levels of miR-155, PI3K, AKT, PI3K, and AKT in U87-MG cells intervened with miR-155 mimic also increased significantly, while the levels of PTEN, Caspase-3, Caspase-9 mRNA, and protein declined significantly, with statistically significant difference. Meanwhile, compared with the control group, miR-155 inhibitor group were on the contrary. Conclusion: The study indicated that miR-155 take charge a key function in regulating the proliferation, migration, and invasion of glioma U87-MG cells through PI3K/AKT signaling pathway, and has anti-glioma effects by inhibition of miR-155, which provided ideas for further clinical treatment of glioma patients. |
format | Online Article Text |
id | pubmed-7198892 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-71988922020-05-14 miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling Wu, Dahao Wang, Changzhen Front Neurol Neurology Objective: Micro-RNA plays a critical role in the pathological process of gliomas. Previous research showed that the level of miR-155 was significantly increased in many cancers, including gliomas. However, the mechanism of glioma is still unknown. Method: To investigate the regulatory function of miR-155 on glioma U87-MG cells and its effects on related signaling pathways. After transfection of miR-155 mimic and inhibitor, the level of miR-155 were applied to detect cell proliferation, apoptosis, senescence index, invasive ability and cell migration at different time points (0, 24, 24 h, respectively) by CCK8 assay, flow cytometry, β-galactosidase (β-gal) staining, transwell and scratch test, respectively. The effect of miR-155 on PI3K/AKT signal pathway was observed at meantime. Results: Compared with the control group, after miR-155 mimic transfection, U87-MG cell viability, cell migration rate and invasiveness were increased, while apoptosis and senescence were significantly decreased, which was the opposite on miR-155 inhibitor transfection. The phosphorylation levels of miR-155, PI3K, AKT, PI3K, and AKT in U87-MG cells intervened with miR-155 mimic also increased significantly, while the levels of PTEN, Caspase-3, Caspase-9 mRNA, and protein declined significantly, with statistically significant difference. Meanwhile, compared with the control group, miR-155 inhibitor group were on the contrary. Conclusion: The study indicated that miR-155 take charge a key function in regulating the proliferation, migration, and invasion of glioma U87-MG cells through PI3K/AKT signaling pathway, and has anti-glioma effects by inhibition of miR-155, which provided ideas for further clinical treatment of glioma patients. Frontiers Media S.A. 2020-04-28 /pmc/articles/PMC7198892/ /pubmed/32411077 http://dx.doi.org/10.3389/fneur.2020.00297 Text en Copyright © 2020 Wu and Wang. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neurology Wu, Dahao Wang, Changzhen miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling |
title | miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling |
title_full | miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling |
title_fullStr | miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling |
title_full_unstemmed | miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling |
title_short | miR-155 Regulates the Proliferation of Glioma Cells Through PI3K/AKT Signaling |
title_sort | mir-155 regulates the proliferation of glioma cells through pi3k/akt signaling |
topic | Neurology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7198892/ https://www.ncbi.nlm.nih.gov/pubmed/32411077 http://dx.doi.org/10.3389/fneur.2020.00297 |
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