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Prazosin inhibits the growth and mobility of osteosarcoma cells
BACKGROUND: Osteosarcoma is a primary malignant bone tumor that frequently occurs in adolescents and children, its high aggressiveness and rapid metastasis often resulting in poor prognoses. In previous studies, Prazosin has been shown to possess anti-proliferative properties against prostate cancer...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AME Publishing Company
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8797549/ https://www.ncbi.nlm.nih.gov/pubmed/35116948 http://dx.doi.org/10.21037/tcr.2019.09.03 |
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author | An, Ming Ma, Wen-Hai Jia, Hong-Wei Li, Yong-Wang Feng, Jing-Jing Meng, Jing Qi, Hui Liu, Jin |
author_facet | An, Ming Ma, Wen-Hai Jia, Hong-Wei Li, Yong-Wang Feng, Jing-Jing Meng, Jing Qi, Hui Liu, Jin |
author_sort | An, Ming |
collection | PubMed |
description | BACKGROUND: Osteosarcoma is a primary malignant bone tumor that frequently occurs in adolescents and children, its high aggressiveness and rapid metastasis often resulting in poor prognoses. In previous studies, Prazosin has been shown to possess anti-proliferative properties against prostate cancer and glioblastoma cells. In our study, we investigated Prazosin’s underlying mechanisms and its effects on the biological behaviors of osteosarcoma cells. METHODS: Osteosarcoma cell lines MG63 and 143B were treated with different concentrations of Prazosin, and a CCK8 assay assessed its effect on cell viability. Colony formation, Transwell and flow cytometry assays were used to examine its effects on cell proliferation, cell migration, and cell invasion and apoptosis, respectively. The expression of relevant proteins was then examined using western blotting. RESULTS: Our data showed that Prazosin dose-dependently reduced the viability of MG63 and 143B cells and significantly inhibited their clonogenic ability. Moreover, Prazosin attenuated the cell migration and invasion abilities of MG63 and 143B cells when compared with the NC group. It also accelerated cell apoptosis in mitochondrial pathways by regulating Bcl-2/Bax axis and caspase 3. Furthermore, Prazosin treatment inactivated the Akt/mTOR pathway by down-regulating Akt and mTOR phosphorylation (p-Akt, p-mTOR) and the expression of P70 and cyclin D1. CONCLUSIONS: Our data highlights the fact that Prazosin inhibits cell growth, inhibits the motility of osteosarcoma cells, and promotes apoptosis, suggesting that Prazosin is a potential anti-cancer agent in osteosarcoma therapy. |
format | Online Article Text |
id | pubmed-8797549 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | AME Publishing Company |
record_format | MEDLINE/PubMed |
spelling | pubmed-87975492022-02-02 Prazosin inhibits the growth and mobility of osteosarcoma cells An, Ming Ma, Wen-Hai Jia, Hong-Wei Li, Yong-Wang Feng, Jing-Jing Meng, Jing Qi, Hui Liu, Jin Transl Cancer Res Original Article BACKGROUND: Osteosarcoma is a primary malignant bone tumor that frequently occurs in adolescents and children, its high aggressiveness and rapid metastasis often resulting in poor prognoses. In previous studies, Prazosin has been shown to possess anti-proliferative properties against prostate cancer and glioblastoma cells. In our study, we investigated Prazosin’s underlying mechanisms and its effects on the biological behaviors of osteosarcoma cells. METHODS: Osteosarcoma cell lines MG63 and 143B were treated with different concentrations of Prazosin, and a CCK8 assay assessed its effect on cell viability. Colony formation, Transwell and flow cytometry assays were used to examine its effects on cell proliferation, cell migration, and cell invasion and apoptosis, respectively. The expression of relevant proteins was then examined using western blotting. RESULTS: Our data showed that Prazosin dose-dependently reduced the viability of MG63 and 143B cells and significantly inhibited their clonogenic ability. Moreover, Prazosin attenuated the cell migration and invasion abilities of MG63 and 143B cells when compared with the NC group. It also accelerated cell apoptosis in mitochondrial pathways by regulating Bcl-2/Bax axis and caspase 3. Furthermore, Prazosin treatment inactivated the Akt/mTOR pathway by down-regulating Akt and mTOR phosphorylation (p-Akt, p-mTOR) and the expression of P70 and cyclin D1. CONCLUSIONS: Our data highlights the fact that Prazosin inhibits cell growth, inhibits the motility of osteosarcoma cells, and promotes apoptosis, suggesting that Prazosin is a potential anti-cancer agent in osteosarcoma therapy. AME Publishing Company 2019-09 /pmc/articles/PMC8797549/ /pubmed/35116948 http://dx.doi.org/10.21037/tcr.2019.09.03 Text en 2019 Translational Cancer Research. All rights reserved. https://creativecommons.org/licenses/by-nc-nd/4.0/Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/. |
spellingShingle | Original Article An, Ming Ma, Wen-Hai Jia, Hong-Wei Li, Yong-Wang Feng, Jing-Jing Meng, Jing Qi, Hui Liu, Jin Prazosin inhibits the growth and mobility of osteosarcoma cells |
title | Prazosin inhibits the growth and mobility of osteosarcoma cells |
title_full | Prazosin inhibits the growth and mobility of osteosarcoma cells |
title_fullStr | Prazosin inhibits the growth and mobility of osteosarcoma cells |
title_full_unstemmed | Prazosin inhibits the growth and mobility of osteosarcoma cells |
title_short | Prazosin inhibits the growth and mobility of osteosarcoma cells |
title_sort | prazosin inhibits the growth and mobility of osteosarcoma cells |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8797549/ https://www.ncbi.nlm.nih.gov/pubmed/35116948 http://dx.doi.org/10.21037/tcr.2019.09.03 |
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