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β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway
Metastatic breast cancer is one of the most common metastatic tumors. Although studies have validated the role of β-inducible gene-h3 (βig-h3) in human biology and disease, the detailed mechanisms mediated by βig-h3 in breast carcinoma metastasis remain unclear. Thus, the present study investigated...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867474/ https://www.ncbi.nlm.nih.gov/pubmed/29599830 http://dx.doi.org/10.3892/etm.2018.5786 |
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author | Zhang, Jiaxin Li, Zhaojiangbo |
author_facet | Zhang, Jiaxin Li, Zhaojiangbo |
author_sort | Zhang, Jiaxin |
collection | PubMed |
description | Metastatic breast cancer is one of the most common metastatic tumors. Although studies have validated the role of β-inducible gene-h3 (βig-h3) in human biology and disease, the detailed mechanisms mediated by βig-h3 in breast carcinoma metastasis remain unclear. Thus, the present study investigated the role and potential mechanism of βig-h3 during breast carcinoma cell metastasis. The results indicated that the upregulation of βig-h3 significantly promotes the growth and inhibits the cisplatin-induced apoptosis of breast carcinoma cells. It was also demonstrated that βig-h3 promoted the migration and invasion of human breast carcinoma cells in vitro and in vivo. Furthermore, the results demonstrated that βig-h3 upregulated the overall expression and phosphorylation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) in human breast carcinoma cells. By contrast, βig-h3 knockdown reversed the βig-h3-mediated characteristics of breast carcinoma cells. Thus, the current study demonstrated that the PI3K/Akt signaling pathway serves a role in βig-h3-induced human breast cancer cell metastasis and that βig-h3 transfection enhances the metastatic potential of human breast carcinoma cells via the PI3K/Akt signaling pathway. These observations contribute to the understanding of the potential mechanism of human breast carcinoma cell growth and metastasis and suggest that βig-h3 may be a promising therapeutic target for the treatment of human breast carcinoma. |
format | Online Article Text |
id | pubmed-5867474 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-58674742018-03-29 β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway Zhang, Jiaxin Li, Zhaojiangbo Exp Ther Med Articles Metastatic breast cancer is one of the most common metastatic tumors. Although studies have validated the role of β-inducible gene-h3 (βig-h3) in human biology and disease, the detailed mechanisms mediated by βig-h3 in breast carcinoma metastasis remain unclear. Thus, the present study investigated the role and potential mechanism of βig-h3 during breast carcinoma cell metastasis. The results indicated that the upregulation of βig-h3 significantly promotes the growth and inhibits the cisplatin-induced apoptosis of breast carcinoma cells. It was also demonstrated that βig-h3 promoted the migration and invasion of human breast carcinoma cells in vitro and in vivo. Furthermore, the results demonstrated that βig-h3 upregulated the overall expression and phosphorylation of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) in human breast carcinoma cells. By contrast, βig-h3 knockdown reversed the βig-h3-mediated characteristics of breast carcinoma cells. Thus, the current study demonstrated that the PI3K/Akt signaling pathway serves a role in βig-h3-induced human breast cancer cell metastasis and that βig-h3 transfection enhances the metastatic potential of human breast carcinoma cells via the PI3K/Akt signaling pathway. These observations contribute to the understanding of the potential mechanism of human breast carcinoma cell growth and metastasis and suggest that βig-h3 may be a promising therapeutic target for the treatment of human breast carcinoma. D.A. Spandidos 2018-03 2018-01-23 /pmc/articles/PMC5867474/ /pubmed/29599830 http://dx.doi.org/10.3892/etm.2018.5786 Text en Copyright: © Zhang 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 Zhang, Jiaxin Li, Zhaojiangbo β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway |
title | β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway |
title_full | β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway |
title_fullStr | β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway |
title_full_unstemmed | β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway |
title_short | β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase B signaling pathway |
title_sort | β-inducible gene-h3 promotes human breast carcinoma cell metastasis by activating the phosphatidylinositol 3-kinase/protein kinase b signaling pathway |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5867474/ https://www.ncbi.nlm.nih.gov/pubmed/29599830 http://dx.doi.org/10.3892/etm.2018.5786 |
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