Abstract
Exploring the biological function of periostin (POSTN) in prostate cancer (PCa) bone metastasis is of importance. It was observed that the expression of POSTN was high in PCa, especially highest in PCa metastasized to bone. In this study, we found that inhibiting POSTN in PCa cells could significantly alleviate PCa bone metastasis in vivo, suggesting POSTN is a promising therapeutic target. Since, due to the secreted expression of POSTN in osteoblasts and PCa, we hypothesized the positive feedback loop between osteoblasts and PCa mediated by POSTN in PCa bone metastasis. The in vitro experiments demonstrated that osteoblast-derived POSTN promoted PCa cell proliferation and invasion and PCa cell-derived POSTN promotes proliferation of osteoblasts. Furthermore, we found that POSTN regulated PCa and osteoblast function through integrin receptors. Finally, 18F-Alfatide II was used as the molecule probe of integrin αvβ3 in PET-CT, revealing high intake in metastatic lesions. Our findings together indicate that targeting POSTN in PCa cells as well as in the osteoblastic may be an effective treatment for PCa bone metastasis.
Highlights
Prostate cancer (PCa) cells possess a propensity to metastasize to bone [1, 2]
Summarizing the previous results, we find that: [1] POSTN is identified in osteoblasts and preferentially expressed in the periosteum as a putative bone adhesion molecule [17, 18]; [2] POSTN is a secreted matricellular protein [31]; [3] POSTN was regulated by Transforming growth factor-b (TGF-b) [25]; [4] POSTN is a ligand of the integrin family [19, 32]; and [5] POSTN promotes epithelialmesenchymal transition (EMT) of PCa cells [33]
Our findings indicate that targeting POSTN in prostate cancer cells as well as in osteoblast may be an effective treatment for PCa bone metastasis
Summary
Prostate cancer (PCa) cells possess a propensity to metastasize to bone [1, 2]. most patients who die from PCa display evidence of bone metastasis [3]. Summarizing the previous results, we find that: [1] POSTN is identified in osteoblasts and preferentially expressed in the periosteum as a putative bone adhesion molecule [17, 18]; [2] POSTN is a secreted matricellular protein [31]; [3] POSTN was regulated by TGF-b [25]; [4] POSTN is a ligand of the integrin family [19, 32]; and [5] POSTN promotes EMT of PCa cells [33] These results together imply POSTN may be a mediator between TGF-b and integrin, which prompt us to explore the role of TGF-b/POSTN/ integrin axis in PCa bone metastasis. Our findings indicate that targeting POSTN in prostate cancer cells as well as in osteoblast may be an effective treatment for PCa bone metastasis
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