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Review
. 2019 Nov 21;39(1):76.
doi: 10.1186/s40880-019-0425-1.

Interactions between cancer cells and bone microenvironment promote bone metastasis in prostate cancer

Affiliations
Review

Interactions between cancer cells and bone microenvironment promote bone metastasis in prostate cancer

Xiangyu Zhang. Cancer Commun (Lond). .

Abstract

Bone metastasis is the leading cause of death in prostate cancer patients, for which there is currently no effective treatment. Since the bone microenvironment plays an important role in this process, attentions have been directed to the interactions between cancer cells and the bone microenvironment, including osteoclasts, osteoblasts, and bone stromal cells. Here, we explained the mechanism of interactions between prostate cancer cells and metastasis-associated cells within the bone microenvironment and further discussed the recent advances in targeted therapy of prostate cancer bone metastasis. This review also summarized the effects of bone microenvironment on prostate cancer metastasis and the related mechanisms, and provides insights for future prostate cancer metastasis studies.

Keywords: Androgen receptor; Bone metastasis; Bone microenvironment; Colonization; Dormancy; Nuclear factor-κB ligand; Prostate cancer; Reactivation; Reconstruction; Targeted therapy.

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Conflict of interest statement

The author declares no competing interests.

Figures

Fig. 1
Fig. 1
Vicious circle in the bone microenvironment of bone metastatic prostate cancer. Prostate cancer cells secrete TGFβ, IGF, PDGF, EDN1, uPA, and VEGF, which regulate osteoblast proliferation and/or differentiation. Osteoblasts secrete RANKL and IL-6 to activate osteoclasts, while OPG can inhibit the activation of osteoclasts, which elicits bone resorption and secrete EGF and calcium, thereby stimulating cancer cell proliferation in bone. Abbreviations: TGFβ, transforming growth factor β; IGF, insulin-like growth factor; PDGF, platelet-derived growth factor; EDN1, endothelin 1; uPA, urokinase plasminogen activator; VEGF, vascular endothelial growth factor; RANKL, receptor activator of the nuclear factor-κB ligand; IL-6, interleukin 6; OPG, osteoprotegerin; EGF, epidermal growth factor

References

    1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2018. CA Cancer J Clin. 2018;68:7–30. doi: 10.3322/caac.21442. - DOI - PubMed
    1. Monn MF, Tatem AJ, Cheng L. Prevalence and management of prostate cancer among East Asian men: current trends and future perspectives. Urol Oncol. 2016;34(2):58. doi: 10.1016/j.urolonc.2015.09.003. - DOI - PubMed
    1. Feng RM, Zong YN, Cao SM, Xu RH. Current cancer situation in China: good or bad news from the 2018 Global Cancer Statistics? Cancer Commun (Lond). 2019;39(1):22. doi: 10.1186/s40880-019-0368-6. - DOI - PMC - PubMed
    1. Nuhn P, de Bono JS, Fizazi K, Freedland SJ, Grilli M, Kantoff PW, et al. Update on systemic prostate cancer therapies: management of metastatic castration-resistant prostate cancer in the era of precision oncology. Eur Urol. 2018;75(1):88–99. doi: 10.1016/j.eururo.2018.03.028. - DOI - PubMed
    1. Peng S, Yi Z, Liu M. Ailanthone: a new potential drug for castration-resistant prostate cancer. Chin J Cancer. 2017;36(1):25. doi: 10.1186/s40880-017-0194-7. - DOI - PMC - PubMed

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