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Prostate‐specific antigen modulates the osteogenic differentiation of MSCs via the cadherin 11‐Akt axis
BACKGROUND: A high prevalence of osteoblastic bone metastases is characteristic of prostate cancer. Prostate‐specific antigen (PSA) is a serine protease uniquely produced by prostate cancer cells and is an important serological marker for prostate cancer. However, whether PSA modulates the osteogeni...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7240859/ https://www.ncbi.nlm.nih.gov/pubmed/32508049 http://dx.doi.org/10.1002/ctm2.27 |
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author | Wu, Longxiang Xiang, Shiqi Hu, Xiheng Mo, Miao Zhao, Cheng Cai, Yi Tong, Shiyu Jiang, Huichuan Chen, Linxiao Wang, Zhi Xiong, Wei Ou, Zhenyu |
author_facet | Wu, Longxiang Xiang, Shiqi Hu, Xiheng Mo, Miao Zhao, Cheng Cai, Yi Tong, Shiyu Jiang, Huichuan Chen, Linxiao Wang, Zhi Xiong, Wei Ou, Zhenyu |
author_sort | Wu, Longxiang |
collection | PubMed |
description | BACKGROUND: A high prevalence of osteoblastic bone metastases is characteristic of prostate cancer. Prostate‐specific antigen (PSA) is a serine protease uniquely produced by prostate cancer cells and is an important serological marker for prostate cancer. However, whether PSA modulates the osteogenic process remains largely unknown. In this study, we explored the effect of PSA on modulating the osteoblastic differentiation of mesenchymal stem cells (MSCs). In this study, we used flow cytometry, CCK‐8 assay, Alizarin red S (ARS) staining and quantification, alkaline phosphatase (ALP) activity and staining, Western blotting, and quantitative real‐time PCR (qRT‐PCR) to explore the effect of PSA on osteogenic differentiation of MSCs. RESULTS: We first demonstrated that although PSA did not affect the proliferation, morphology, or phenotype of MSCs, it significantly promoted the osteogenic differentiation of MSCs in a concentration‐dependent manner. Furthermore, we demonstrated that PSA promoted the osteogenic differentiation of MSCs by elevating the expression of Cadherin 11 in MSCs and, thus, activating the Akt signaling pathway. CONCLUSIONS: In conclusion, we demonstrated that PSA could promote the osteogenesis of MSCs through Akt signaling pathway activation by elevating the expression of cadherin‐11 in MSCs. These findings imply a possible role of PSA in osteoblastic bone metastases in prostate cancer. |
format | Online Article Text |
id | pubmed-7240859 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-72408592020-06-01 Prostate‐specific antigen modulates the osteogenic differentiation of MSCs via the cadherin 11‐Akt axis Wu, Longxiang Xiang, Shiqi Hu, Xiheng Mo, Miao Zhao, Cheng Cai, Yi Tong, Shiyu Jiang, Huichuan Chen, Linxiao Wang, Zhi Xiong, Wei Ou, Zhenyu Clin Transl Med Research Articles BACKGROUND: A high prevalence of osteoblastic bone metastases is characteristic of prostate cancer. Prostate‐specific antigen (PSA) is a serine protease uniquely produced by prostate cancer cells and is an important serological marker for prostate cancer. However, whether PSA modulates the osteogenic process remains largely unknown. In this study, we explored the effect of PSA on modulating the osteoblastic differentiation of mesenchymal stem cells (MSCs). In this study, we used flow cytometry, CCK‐8 assay, Alizarin red S (ARS) staining and quantification, alkaline phosphatase (ALP) activity and staining, Western blotting, and quantitative real‐time PCR (qRT‐PCR) to explore the effect of PSA on osteogenic differentiation of MSCs. RESULTS: We first demonstrated that although PSA did not affect the proliferation, morphology, or phenotype of MSCs, it significantly promoted the osteogenic differentiation of MSCs in a concentration‐dependent manner. Furthermore, we demonstrated that PSA promoted the osteogenic differentiation of MSCs by elevating the expression of Cadherin 11 in MSCs and, thus, activating the Akt signaling pathway. CONCLUSIONS: In conclusion, we demonstrated that PSA could promote the osteogenesis of MSCs through Akt signaling pathway activation by elevating the expression of cadherin‐11 in MSCs. These findings imply a possible role of PSA in osteoblastic bone metastases in prostate cancer. John Wiley and Sons Inc. 2020-05-15 /pmc/articles/PMC7240859/ /pubmed/32508049 http://dx.doi.org/10.1002/ctm2.27 Text en © 2020 The Authors. Clinical and Translational Medicine published by John Wiley & Sons Australia, Ltd on behalf of Shanghai Institute of Clinical Bioinformatics This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Articles Wu, Longxiang Xiang, Shiqi Hu, Xiheng Mo, Miao Zhao, Cheng Cai, Yi Tong, Shiyu Jiang, Huichuan Chen, Linxiao Wang, Zhi Xiong, Wei Ou, Zhenyu Prostate‐specific antigen modulates the osteogenic differentiation of MSCs via the cadherin 11‐Akt axis |
title | Prostate‐specific antigen modulates the osteogenic differentiation of MSCs via the cadherin 11‐Akt axis |
title_full | Prostate‐specific antigen modulates the osteogenic differentiation of MSCs via the cadherin 11‐Akt axis |
title_fullStr | Prostate‐specific antigen modulates the osteogenic differentiation of MSCs via the cadherin 11‐Akt axis |
title_full_unstemmed | Prostate‐specific antigen modulates the osteogenic differentiation of MSCs via the cadherin 11‐Akt axis |
title_short | Prostate‐specific antigen modulates the osteogenic differentiation of MSCs via the cadherin 11‐Akt axis |
title_sort | prostate‐specific antigen modulates the osteogenic differentiation of mscs via the cadherin 11‐akt axis |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7240859/ https://www.ncbi.nlm.nih.gov/pubmed/32508049 http://dx.doi.org/10.1002/ctm2.27 |
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