ArticleJournal of thrombosis and haemostasis : JTH2022
Breast cancer cells mediate endothelial cell activation, promoting von Willebrand factor release, tumor adhesion, and transendothelial migration.
Article in Journal of thrombosis and haemostasis : JTH, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 49 citations in OpenAlex.
- The Cancer Immunotherapy Thromboembolism Assessment: A Novel Score for Predicting Thromboembolic Events in Melanoma Patients Treated With Immune Checkpoint Inhibition.International journal of cancer · 2026Article
- Shear-Activated von Willebrand Factor Captures Extracellular Vesicles to Promote Platelet Activation and Metastasis.Journal of extracellular vesicles · 2026Article
- Breast Cancer-Associated Venous Thromboembolism: Risk Factors, Mechanisms, and Clinical Management.Cancers · 2026Review
- Protein Kinase C-Delta (PKCδ) inhibition stabilizes endothelium and suppresses triple-negative breast cancer (TNBC) intravasation in a microfluidic hypoxic tumor model.Bioengineering & translational medicine · 2026Article
- Mechanobiology of cancer-associated thrombosis: from molecular mechanisms to therapeutic innovation.Journal of nanobiotechnology · 2026Review
- Mitochondrial IκBα fuels cancer progression through metabolic rewiring, endothelial activation, and thrombotic spread.Cell death discovery · 2026Article
- Thrombotic Thrombocytopenic Purpura in a Patient With Triple-Negative Breast Cancer Treated With PD-L1 Inhibition and Taxane Chemotherapy.Clinical case reports · 2026Article
- Structure and multiple functions of von Willebrand factor.Haematologica · 2026Review
- Engineering Complexity: Advances in 3D Breast Cancer Models for Precision Oncology.Advanced healthcare materials · 2026Review
- Article
- Emerging roles of haemostatic proteins as markers of disease progression and prognosis in breast cancer.Exploration of targeted anti-tumor therapy · 2026Review
- Heparin, Heparin-like Molecules, and Heparin Mimetics in Breast Cancer: A Concise Review.Biomolecules · 2025Review
- Venous Thromboembolic Events in Cancer Immunotherapy: A Narrative Review.Journal of clinical medicine · 2025Review
- Crosstalk between GLTSCR1-deficient endothelial cells and tumour cells promotes colorectal cancer development by activating the Notch pathway.Cell death and differentiation · 2025Article
- Platelet activation in breast cancer: mechanisms and therapeutic opportunities - a narrative review.Annals of medicine and surgery (2012) · 2025Review
- Breaking the premetastatic niche barrier: the role of endothelial cells and therapeutic strategies.Theranostics · 2025Review
- AKAP12 Variant 1 Knockout Enhances Vascular Endothelial Cell Motility.Journal of vascular research · 2025Article
- Plasma von Willebrand factor levels in patients with cancer: A meta‑analysis.Oncology letters · 2024Article
- Microsphere-Enabled Modular Formation of Miniaturized In Vitro Breast Cancer Models.Small (Weinheim an der Bergstrasse, Germany) · 2024Article
- Extracellular vesicles derived from SARS-CoV-2 M-protein-induced triple negative breast cancer cells promoted the ability of tissue stem cells supporting cancer progression.Frontiers in oncology · 2024Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBreast cancer results in a three- to four-fold increased risk of venous thromboembolism (VTE), which is associated with reduced patient survival. Despite this, the mechanisms underpinning breast cancer-associated thrombosis remain poorly defined. Tumor cells can trigger endothelial cell (EC) activation resulting in increased von Willebrand factor (VWF) secretion. Importantly, elevated plasma VWF levels constitute an independent biomarker for VTE risk. Moreover, in a model of melanoma, treatment with low molecular weight heparin (LMWH) negatively regulated VWF secretion and attenuated tumor metastasis.
objectiveTo investigate the role of VWF in breast cancer metastasis and examine the effect of LMWH in modulating EC activation and breast tumor transmigration.
methodsvon Willebrand factor levels were measured by ELISA. Primary ECs were used to assess tumor-induced activation, angiogenesis, tumor adhesion, and transendothelial migration. RESULTS AND
conclusionPatients with metastatic breast cancer have markedly elevated plasma VWF:Ag levels that also correlate with poorer survival. MDA-MB-231 and MCF-7 breast cancer cells induce secretion of VWF, angiopoietin-2, and osteoprotegerin from ECs, which is further enhanced by the presence of platelets. Vascular endothelial growth factor-A (VEGF-A) plays an important role in modulating breast cancer-induced VWF release. Moreover, VEGF-A from breast tumor cells also contributes to a pro-angiogenic effect on ECs. VWF multimers secreted from ECs, in response to tumor-VEGF-A, mediate adhesion of breast tumor cells along the endothelium. LMWH inhibits VWF-breast tumor adhesion and transendothelial migration. Our findings highlight the significant crosstalk between tumor cells and the endothelium including increased VWF secretion which may contribute to tumor metastasis.
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