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Prostate Cancer Bone Metastasis: Molecular Mechanisms of Tumor and Bone Microenvironment.

作者信息

Jiang Hua

机构信息

Department of Urology, Fifth Affiliated Hospital of Zunyi Medical University (Zhuhai Sixth People's Hospital), Zhuhai, People's Republic of China.

出版信息

Cancer Manag Res. 2025 Feb 1;17:219-237. doi: 10.2147/CMAR.S495169. eCollection 2025.


DOI:10.2147/CMAR.S495169
PMID:39912095
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11796448/
Abstract

Prostate cancer is prevalent among men aged 65 and older. Bone metastasis occurs in up to 90% of advanced prostate cancer patients, metastatic prostate cancer is generally considered a non-curative condition which can impact quality of life. The tumor microenvironment, comprising diverse cellular and non-cellular elements, interacts with prostate cancer cells to affect tumor growth and bone metastasis. Within the bone microenvironment, different cell types, including osteoblasts, osteoclasts, adipocytes, endothelial cells, hematopoietic stem cells, and immune cells, engage with tumor cells. Some cells alter tumor behavior, while others are impacted or overpowered by tumor cells, leading to different phases of tumor cell movement, dormancy, latency, resistance to treatment, and advancement to visible bone metastasis. This review summarizes recent research on the tumor microenvironment and bone microenvironment in prostate cancer bone metastasis, exploring underlying mechanisms and the potential value of targeting these environments for treatment.

摘要
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/634a/11796448/0f7b95b14927/CMAR-17-219-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/634a/11796448/95756ac8d182/CMAR-17-219-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/634a/11796448/3443f94d8b11/CMAR-17-219-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/634a/11796448/0f7b95b14927/CMAR-17-219-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/634a/11796448/95756ac8d182/CMAR-17-219-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/634a/11796448/3443f94d8b11/CMAR-17-219-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/634a/11796448/0f7b95b14927/CMAR-17-219-g0003.jpg

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[1]
Prostate Cancer Bone Metastasis: Molecular Mechanisms of Tumor and Bone Microenvironment.

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[2]
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[3]
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[4]
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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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引用本文的文献

[1]
From Hypoxia to Bone: Reprogramming the Prostate Cancer Metastatic Cascade.

Int J Mol Sci. 2025-8-1

本文引用的文献

[1]
Bone metastasis in endocrine-related cancer: unravelling invasion and destruction.

Endocr Relat Cancer. 2025-1-11

[2]
An immune suppressive tumor microenvironment in primary prostate cancer promotes tumor immune escape.

PLoS One. 2024

[3]
Role of Chemokines and Cytokines in Prostate Cancer Skeletal Metastasis.

Curr Osteoporos Rep. 2024-11-25

[4]
Phase II trial of multi-tyrosine kinase inhibitor ESK981 in combination with PD-1 inhibitor nivolumab in patients with metastatic castration-resistant prostate cancer.

Invest New Drugs. 2024-12

[5]
Insight into prostate cancer osteolytic metastasis by RelB coordination of IL-8 and S100A4.

Clin Transl Med. 2024-10

[6]
The Immune Microenvironment in Prostate Cancer: A Comprehensive Review.

Oncology. 2024-10-9

[7]
WNT5A is a putative epi-driver of prostate cancer metastasis to the bone.

Cancer Med. 2024-8

[8]
Expression of the αVβ3 integrin affects prostate cancer sEV cargo and density and promotes sEV pro-tumorigenic activity in vivo through a GPI-anchored receptor, NgR2.

J Extracell Vesicles. 2024-8

[9]
Prostate cancer-induced endothelial-cell-to-osteoblast transition drives immunosuppression in the bone-tumor microenvironment through Wnt pathway-induced M2 macrophage polarization.

Proc Natl Acad Sci U S A. 2024-8-13

[10]
Cancer-associated fibroblasts and prostate cancer stem cells: crosstalk mechanisms and implications for disease progression.

Front Cell Dev Biol. 2024-7-18

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