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TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway
BACKGROUND: The transforming growth factor β regulator 4 (TBRG4) has been proved to be involved in various types of tumor. However, its contribution in human osteosarcoma (OS) is still unclear. PATIENTS AND METHODS: In the present study, immunohistochemistry and quantitative real-time PCR were perfo...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7394601/ https://www.ncbi.nlm.nih.gov/pubmed/32801755 http://dx.doi.org/10.2147/OTT.S249477 |
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author | Huang, Fei Liao, Faxue Ma, Guangwen Hu, Yong Zhang, Chi Xu, Pengfei Xu, Tangbing Chang, Jun |
author_facet | Huang, Fei Liao, Faxue Ma, Guangwen Hu, Yong Zhang, Chi Xu, Pengfei Xu, Tangbing Chang, Jun |
author_sort | Huang, Fei |
collection | PubMed |
description | BACKGROUND: The transforming growth factor β regulator 4 (TBRG4) has been proved to be involved in various types of tumor. However, its contribution in human osteosarcoma (OS) is still unclear. PATIENTS AND METHODS: In the present study, immunohistochemistry and quantitative real-time PCR were performed to investigate the expression of TBRG4 in OS tissues obtained from patients and three types of cell lines. The effect of TBRG4 knockdown using lentivirus on tumorigenesis was detected by CCK8, high-content screening analysis, colony formation assay and flow cytometric analysis. Bioinformatics analysis was operated to investigate related signaling pathways following TBRG4 knockdown. RESULTS: The results showed that the expression of TBRG4 increased significantly in OS tissues and MG63 cell line. TBRG4 knockdown inhibited cell proliferation, colony and tumor formation, while activating cell apoptosis. Ingenuity Pathway Analysis and Western blot assay further indicated that TBRG4 knockdown may regulate the proliferation of human MG63 cells through PI3K/Akt signaling pathway. CONCLUSION: Our results suggest that TBRG4 may become a promising therapeutic target for the treatment of human OS. |
format | Online Article Text |
id | pubmed-7394601 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | Dove |
record_format | MEDLINE/PubMed |
spelling | pubmed-73946012020-08-13 TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway Huang, Fei Liao, Faxue Ma, Guangwen Hu, Yong Zhang, Chi Xu, Pengfei Xu, Tangbing Chang, Jun Onco Targets Ther Original Research BACKGROUND: The transforming growth factor β regulator 4 (TBRG4) has been proved to be involved in various types of tumor. However, its contribution in human osteosarcoma (OS) is still unclear. PATIENTS AND METHODS: In the present study, immunohistochemistry and quantitative real-time PCR were performed to investigate the expression of TBRG4 in OS tissues obtained from patients and three types of cell lines. The effect of TBRG4 knockdown using lentivirus on tumorigenesis was detected by CCK8, high-content screening analysis, colony formation assay and flow cytometric analysis. Bioinformatics analysis was operated to investigate related signaling pathways following TBRG4 knockdown. RESULTS: The results showed that the expression of TBRG4 increased significantly in OS tissues and MG63 cell line. TBRG4 knockdown inhibited cell proliferation, colony and tumor formation, while activating cell apoptosis. Ingenuity Pathway Analysis and Western blot assay further indicated that TBRG4 knockdown may regulate the proliferation of human MG63 cells through PI3K/Akt signaling pathway. CONCLUSION: Our results suggest that TBRG4 may become a promising therapeutic target for the treatment of human OS. Dove 2020-07-27 /pmc/articles/PMC7394601/ /pubmed/32801755 http://dx.doi.org/10.2147/OTT.S249477 Text en © 2020 Huang et al. http://creativecommons.org/licenses/by-nc/3.0/ This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms (https://www.dovepress.com/terms.php). |
spellingShingle | Original Research Huang, Fei Liao, Faxue Ma, Guangwen Hu, Yong Zhang, Chi Xu, Pengfei Xu, Tangbing Chang, Jun TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway |
title | TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway |
title_full | TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway |
title_fullStr | TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway |
title_full_unstemmed | TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway |
title_short | TBRG4 Knockdown Suppresses Proliferation and Growth of Human Osteosarcoma Cell Lines MG63 Through PI3K/Akt Pathway |
title_sort | tbrg4 knockdown suppresses proliferation and growth of human osteosarcoma cell lines mg63 through pi3k/akt pathway |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7394601/ https://www.ncbi.nlm.nih.gov/pubmed/32801755 http://dx.doi.org/10.2147/OTT.S249477 |
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