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前列腺特异性抗原通过钙黏蛋白11-Akt轴调节间充质干细胞的成骨分化。

Prostate-specific antigen modulates the osteogenic differentiation of MSCs via the cadherin 11-Akt axis.

作者信息

Wu Longxiang, Xiang Shiqi, Hu Xiheng, Mo Miao, Zhao Cheng, Cai Yi, Tong Shiyu, Jiang Huichuan, Chen Linxiao, Wang Zhi, Xiong Wei, Ou Zhenyu

机构信息

Department of Urology, Xiangya Hospital of Central South University, Changsha, P.R. China.

Department of Orthopedics, The Second Xiangya Hospital of Central South University, Changsha, P.R. China.

出版信息

Clin Transl Med. 2020 Jan;10(1):363-373. doi: 10.1002/ctm2.27.

DOI:10.1002/ctm2.27
PMID:32508049
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7240859/
Abstract

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.

摘要

背景

成骨性骨转移的高发生率是前列腺癌的特征。前列腺特异性抗原（PSA）是前列腺癌细胞独特产生的一种丝氨酸蛋白酶，是前列腺癌的重要血清学标志物。然而，PSA是否调节成骨过程在很大程度上仍不清楚。在本研究中，我们探讨了PSA对间充质干细胞（MSCs）成骨分化的调节作用。在本研究中，我们使用流式细胞术、CCK-8 检测、茜素红 S（ARS）染色及定量、碱性磷酸酶（ALP）活性及染色、蛋白质印迹法和定量实时聚合酶链反应（qRT-PCR）来探讨PSA对MSCs成骨分化的影响。

结果

我们首先证明，尽管PSA不影响MSCs的增殖、形态或表型，但它以浓度依赖的方式显著促进了MSCs的成骨分化。此外，我们证明PSA通过提高MSCs中钙黏蛋白11的表达，从而激活Akt信号通路，促进了MSCs的成骨分化。

结论

总之，我们证明PSA可通过提高MSCs中钙黏蛋白11的表达激活Akt信号通路，从而促进MSCs的成骨作用。这些发现暗示了PSA在前列腺癌成骨性骨转移中的可能作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1813/7240859/47b46140f3d0/CTM2-10-363-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1813/7240859/7274a1bb643b/CTM2-10-363-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1813/7240859/47b46140f3d0/CTM2-10-363-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1813/7240859/7274a1bb643b/CTM2-10-363-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1813/7240859/6b9d482000b5/CTM2-10-363-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1813/7240859/6124d3d0273e/CTM2-10-363-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1813/7240859/c274a45147a4/CTM2-10-363-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1813/7240859/1761670786fd/CTM2-10-363-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1813/7240859/47b46140f3d0/CTM2-10-363-g006.jpg

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