ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
Cancer Cell-Derived Large Extracellular Vesicles Promote Venous Thromboembolism by Activating NETosis Through Delivering CYBA.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- An Immunothrombotic Extracellular Vesicle mRNA Profile Associated with Thrombosis in Lung Adenocarcinoma.International journal of molecular sciences · 2026Article
- Transcriptomic Profiling and WGCNA Identify ALOX5 as a Key Regulator of Iron Metabolism and Immune Crosstalk in Venous Thromboembolism.Current issues in molecular biology · 2026Article
- Neutrophil Extracellular Traps in Diabetic Kidney Disease: Mechanisms of Pathogenesis and Emerging Therapeutic Strategies.Drug design, development and therapy · 2026Review
- Cancer Cell-Derived Large Extracellular Vesicles Promote Venous Thromboembolism by Activating NETosis Through Delivering CYBA.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Pan-cancer single-cell transcriptomic analysis reveals CD83 as a hallmark of tumor-associated neutrophils with senescent and pro-tumor properties.Computational and structural biotechnology journal · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
Venous thromboembolism (VTE) is the second-leading cause of cancer-associated mortality. Neutrophil extracellular trap formation (i.e., NETosis) is a crucial process in forming VTE in cancer patients. Nevertheless, how cancer cells contribute to NETosis remains unclear. This study investigated the potential activation effects of cancer cell-derived extracellular vesicles (CC-EVs) on neutrophils. Both small and large EVs (sEVs and lEVs) released from cancer cells are found to significantly induce NETosis in neutrophil-like HL-60 (dHL-60) cells. Following an in-depth exploration of EV-induced NETosis, the specific molecular pathways involved in this biological process are elucidated. CYBA enriched in CC-lEVs is delivered to dHL-60, leading to a rapid increase in intracellular ROS levels and upregulation of citH3 expression. This cascade resulted in decondensed chromatin release and subsequent NETosis along with elevated MPO-DNA levels. Injection of CC-lEVs into mice caused more pronounced VTE, which is accompanied by increased peripheral blood levels of the MPO-DNA and thrombin-antithrombin complex. Inhibiting CYBA expression or ROS generation prevented NETosis in vitro and significantly reduced VTE in vivo. In conclusion, CC-lEVs induce NETosis through the CYBA-ROS-citH3 pathway and increase VTE risk. Targeting CYBA expression or ROS production can provide novel strategies for preventing and treating VTE in high-risk cancer patients.
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Registered trials
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