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miR-22 promotes apoptosis of osteosarcoma cells via inducing cell cycle arrest

To study the effects of miR-22 on the proliferation and the apoptosis of osteosarcoma MG-63 cell line and to explore the potential molecular mechanism that miR-22 regulates this biological process. Quantitive real-time polymerase chain reaction (RT-qPCR) was performed to explore the miRNA level of m...

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Autores principales: Gai, Pengzhou, Sun, Hongliang, Wang, Guangda, Xu, Qiang, Qi, Xiaojun, Zhang, Zuofu, Jiang, Lei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403490/
https://www.ncbi.nlm.nih.gov/pubmed/28454403
http://dx.doi.org/10.3892/ol.2017.5674
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author Gai, Pengzhou
Sun, Hongliang
Wang, Guangda
Xu, Qiang
Qi, Xiaojun
Zhang, Zuofu
Jiang, Lei
author_facet Gai, Pengzhou
Sun, Hongliang
Wang, Guangda
Xu, Qiang
Qi, Xiaojun
Zhang, Zuofu
Jiang, Lei
author_sort Gai, Pengzhou
collection PubMed
description To study the effects of miR-22 on the proliferation and the apoptosis of osteosarcoma MG-63 cell line and to explore the potential molecular mechanism that miR-22 regulates this biological process. Quantitive real-time polymerase chain reaction (RT-qPCR) was performed to explore the miRNA level of miR-22. The MG-63 cell line was infected with miR-22 mimics for establishment of miR-22 overexpression. Non-infected cells were in blank group and cells infected with empty vector were served as negative control (NC group). MTT assay was conducted to measure cell viability. The cell cycle and apoptosis were explored using flow cytometry and the apoptosis-related markers were detected by western blotting. RT-qPCR results revealed that the miR-22 miRNA level in the MG-63 cells was significantly lower than that in osteoblasts (P<0.05). MTT assay showed that the MG-63 cells infected with miR-22 mimics exhibited markedly decreased proliferation ability compared with blank and empty vector (NC) groups. Next, we found that overexpression of miR-22 remarkably increased the apoptosis of the MG-63 cells, evidenced from the flow cytometry results and elevated Bax and reduced Bcl-2. Furthermore, results revealed that percentage of the cells at G0/G1 phase in miR-22 mimic group (66.75±3.67%) was significantly higher than blank (52.9±2.58%) and NC (50.5±2.45%) groups. miR-22 attenuated the proliferation and induced the apoptosis of the MG-63 cells via promoting G0/G1 cell cycle arrest. Thus, miR-22 may have the potential to be a novel therapeutic in treatment of osteosarcoma.
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spelling pubmed-54034902017-04-27 miR-22 promotes apoptosis of osteosarcoma cells via inducing cell cycle arrest Gai, Pengzhou Sun, Hongliang Wang, Guangda Xu, Qiang Qi, Xiaojun Zhang, Zuofu Jiang, Lei Oncol Lett Articles To study the effects of miR-22 on the proliferation and the apoptosis of osteosarcoma MG-63 cell line and to explore the potential molecular mechanism that miR-22 regulates this biological process. Quantitive real-time polymerase chain reaction (RT-qPCR) was performed to explore the miRNA level of miR-22. The MG-63 cell line was infected with miR-22 mimics for establishment of miR-22 overexpression. Non-infected cells were in blank group and cells infected with empty vector were served as negative control (NC group). MTT assay was conducted to measure cell viability. The cell cycle and apoptosis were explored using flow cytometry and the apoptosis-related markers were detected by western blotting. RT-qPCR results revealed that the miR-22 miRNA level in the MG-63 cells was significantly lower than that in osteoblasts (P<0.05). MTT assay showed that the MG-63 cells infected with miR-22 mimics exhibited markedly decreased proliferation ability compared with blank and empty vector (NC) groups. Next, we found that overexpression of miR-22 remarkably increased the apoptosis of the MG-63 cells, evidenced from the flow cytometry results and elevated Bax and reduced Bcl-2. Furthermore, results revealed that percentage of the cells at G0/G1 phase in miR-22 mimic group (66.75±3.67%) was significantly higher than blank (52.9±2.58%) and NC (50.5±2.45%) groups. miR-22 attenuated the proliferation and induced the apoptosis of the MG-63 cells via promoting G0/G1 cell cycle arrest. Thus, miR-22 may have the potential to be a novel therapeutic in treatment of osteosarcoma. D.A. Spandidos 2017-04 2017-02-02 /pmc/articles/PMC5403490/ /pubmed/28454403 http://dx.doi.org/10.3892/ol.2017.5674 Text en Copyright: © Gai et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Gai, Pengzhou
Sun, Hongliang
Wang, Guangda
Xu, Qiang
Qi, Xiaojun
Zhang, Zuofu
Jiang, Lei
miR-22 promotes apoptosis of osteosarcoma cells via inducing cell cycle arrest
title miR-22 promotes apoptosis of osteosarcoma cells via inducing cell cycle arrest
title_full miR-22 promotes apoptosis of osteosarcoma cells via inducing cell cycle arrest
title_fullStr miR-22 promotes apoptosis of osteosarcoma cells via inducing cell cycle arrest
title_full_unstemmed miR-22 promotes apoptosis of osteosarcoma cells via inducing cell cycle arrest
title_short miR-22 promotes apoptosis of osteosarcoma cells via inducing cell cycle arrest
title_sort mir-22 promotes apoptosis of osteosarcoma cells via inducing cell cycle arrest
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5403490/
https://www.ncbi.nlm.nih.gov/pubmed/28454403
http://dx.doi.org/10.3892/ol.2017.5674
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