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MicroRNA16 regulates glioma cell proliferation, apoptosis and invasion by targeting Wip1-ATM-p53 feedback loop

The present study aimed to investigate the role and underlying mechanisms of microRNA16 (miR-16) on proliferation, apoptosis and invasion of glioma cells. The cell models of miR-16 upregulation and Negative control group (NC group) were built. The cell functions of different groups were detected by...

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Autores principales: Zhan, Xiao-Hong, Xu, Qiu-Yan, Tian, Rui, Yan, Hong, Zhang, Min, Wu, Jing, Wang, Wei, He, Jie
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5589621/
https://www.ncbi.nlm.nih.gov/pubmed/28903382
http://dx.doi.org/10.18632/oncotarget.18510
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author Zhan, Xiao-Hong
Xu, Qiu-Yan
Tian, Rui
Yan, Hong
Zhang, Min
Wu, Jing
Wang, Wei
He, Jie
author_facet Zhan, Xiao-Hong
Xu, Qiu-Yan
Tian, Rui
Yan, Hong
Zhang, Min
Wu, Jing
Wang, Wei
He, Jie
author_sort Zhan, Xiao-Hong
collection PubMed
description The present study aimed to investigate the role and underlying mechanisms of microRNA16 (miR-16) on proliferation, apoptosis and invasion of glioma cells. The cell models of miR-16 upregulation and Negative control group (NC group) were built. The cell functions of different groups were detected by colony formation assay, transwell chamber assay, proliferation, apoptosis and cycle experiments. The intracranial orthotopic transplantation animal models were built to different groups: miR-16 agomir group, miR-16 antagomir group and their NC group. The expressions of miR-16, Wip1, ATM and p53 were measured by qRT-PCR, western blot and immunohistochemistry. As a result, miR-16 overexpressed groups had lower cloning formation rate and proliferation rate, less invasive cells, higher early apoptosis rate than the control groups. G1 phase was significantly smaller compared miR-16 overexpressed groups with the control groups, and S phase significantly lesser. Cell growth was retardated. Differences were statistically significant (P <0.05). Compared with miR-16 overexpressed groups and NC groups, the Wip1 gene and protein expression were downregulated, while ATM and p53 genes, p-ATM and p-p53 proteins were upregulated. The differences were statistically significant (P <0.05). Taken together, our findings demonstrated that miR-16 suppressed glioma cell proliferation and invasion, promoted apoptosis and inhibited cell cycle by targeting Wip1-ATM-p53 signaling pathway.
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spelling pubmed-55896212017-09-12 MicroRNA16 regulates glioma cell proliferation, apoptosis and invasion by targeting Wip1-ATM-p53 feedback loop Zhan, Xiao-Hong Xu, Qiu-Yan Tian, Rui Yan, Hong Zhang, Min Wu, Jing Wang, Wei He, Jie Oncotarget Research Paper The present study aimed to investigate the role and underlying mechanisms of microRNA16 (miR-16) on proliferation, apoptosis and invasion of glioma cells. The cell models of miR-16 upregulation and Negative control group (NC group) were built. The cell functions of different groups were detected by colony formation assay, transwell chamber assay, proliferation, apoptosis and cycle experiments. The intracranial orthotopic transplantation animal models were built to different groups: miR-16 agomir group, miR-16 antagomir group and their NC group. The expressions of miR-16, Wip1, ATM and p53 were measured by qRT-PCR, western blot and immunohistochemistry. As a result, miR-16 overexpressed groups had lower cloning formation rate and proliferation rate, less invasive cells, higher early apoptosis rate than the control groups. G1 phase was significantly smaller compared miR-16 overexpressed groups with the control groups, and S phase significantly lesser. Cell growth was retardated. Differences were statistically significant (P <0.05). Compared with miR-16 overexpressed groups and NC groups, the Wip1 gene and protein expression were downregulated, while ATM and p53 genes, p-ATM and p-p53 proteins were upregulated. The differences were statistically significant (P <0.05). Taken together, our findings demonstrated that miR-16 suppressed glioma cell proliferation and invasion, promoted apoptosis and inhibited cell cycle by targeting Wip1-ATM-p53 signaling pathway. Impact Journals LLC 2017-06-16 /pmc/articles/PMC5589621/ /pubmed/28903382 http://dx.doi.org/10.18632/oncotarget.18510 Text en Copyright: © 2017 Zhan et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (http://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Zhan, Xiao-Hong
Xu, Qiu-Yan
Tian, Rui
Yan, Hong
Zhang, Min
Wu, Jing
Wang, Wei
He, Jie
MicroRNA16 regulates glioma cell proliferation, apoptosis and invasion by targeting Wip1-ATM-p53 feedback loop
title MicroRNA16 regulates glioma cell proliferation, apoptosis and invasion by targeting Wip1-ATM-p53 feedback loop
title_full MicroRNA16 regulates glioma cell proliferation, apoptosis and invasion by targeting Wip1-ATM-p53 feedback loop
title_fullStr MicroRNA16 regulates glioma cell proliferation, apoptosis and invasion by targeting Wip1-ATM-p53 feedback loop
title_full_unstemmed MicroRNA16 regulates glioma cell proliferation, apoptosis and invasion by targeting Wip1-ATM-p53 feedback loop
title_short MicroRNA16 regulates glioma cell proliferation, apoptosis and invasion by targeting Wip1-ATM-p53 feedback loop
title_sort microrna16 regulates glioma cell proliferation, apoptosis and invasion by targeting wip1-atm-p53 feedback loop
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5589621/
https://www.ncbi.nlm.nih.gov/pubmed/28903382
http://dx.doi.org/10.18632/oncotarget.18510
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