ArticleFrontiers in oncology2023
Extracellular vesicles secreted from bone metastatic renal cell carcinoma promote angiogenesis and endothelial gap formation in bone marrow in a time-dependent manner in a preclinical mouse model.
Article in Frontiers in oncology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- 3D co-culture model of tumor spheroid and endothelial cells unveils ccRCC aberrant vasculature and distinct sensitivity to targeted treatments.Angiogenesis · 2026Article
- Orchestrating Tumor Metastasis: Exosomes as Master Regulators of the Local and Distant Microenvironment.International journal of biological sciences · 2026Review
- Predictors of early progressive disease and antitumor effects by metastatic site in renal cell carcinoma treated with ipilimumab plus nivolumab.International journal of clinical oncology · 2025Article
- Exploring molecular and cellular mechanisms of Pre-Metastatic niche in renal cell carcinoma.Molecular cancer · 2025Review
- New players in the landscape of renal cell carcinoma bone metastasis and therapeutic opportunities.International journal of cancer · 2025Review
- Research advances of tissue-derived extracellular vesicles in cancers.Journal of cancer research and clinical oncology · 2024Review
- The Roles of Extracellular Vesicles in the Progression of Renal Cell Carcinoma and Their Potential for Future Clinical Application.Nanomaterials (Basel, Switzerland) · 2023Review
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
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Abstract
Introduction: Bone is a major metastatic site of renal cell carcinoma (RCC). Recently, it is well recognized that bone metastatic tumor cells remodel bone marrow vasculature. However, the precise mechanism underlying cell-cell communication between bone metastatic RCC and the cells in bone marrow remains unknown. Extracellular vesicles (EVs) reportedly play crucial roles in intercellular communication between metastatic tumor cells and bone marrow. Therefore, we conducted the current study to clarify the histological alteration in vascular endothelium in bone marrow induced by EVs secreted from bone metastatic RCC cells as well as association between angiogenesis in bone marrow and bone metastasis formation. Materials and methods: We established a bone metastatic RCC cell line (786-O BM) by in vivo selection and observed phenotypic changes in tissues when EVs were intravenously injected into immunodeficient mice. Proteomic analysis was performed to identify the protein cargo of EVs that could contribute to histological changes in bone. Tissue exudative EVs (Te-EVs) from cancer tissues of patients with bone metastatic RCC (BM-EV) and those with locally advanced disease (LA-EV) were compared for in vitro function and protein cargo. Results: Treatment of mice with EVs from 786-O BM promoted angiogenesis in the bone marrow in a time-dependent manner and increased the gaps of capillary endothelium. 786-O BM EVs also promoted tube formation Conclusion: EVs from bone metastatic RCC promote angiogenesis and gap formation in capillary endothelium in bone marrow in a time-dependent manner.
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