ArticleCellular & molecular immunology2025
The NET-DNA-CCDC25 inhibitor di-Pal-MTO suppresses tumor progression and promotes the innate immune response.
Article in Cellular & molecular immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Neutrophil extracellular traps promote liver metastasis by impairing NK cell-dependent tumor surveillance via CCDC25.Nature communications · 2026Article
- Roles of neutrophil extracellular traps in cancer immunotherapy resistance and therapeutic targeting.Biomarker research · 2026Review
- SREBP2 regulates CCDC25 expression and promotes tumor metastasis in Triple-Negative Breast Cancer.Oncogenesis · 2026Article
- Neutrophil Extracellular Traps in Cancer Metastasis: From Mechanistic Understanding to Targeted Therapy.Current oncology (Toronto, Ont.) · 2026Review
- Tumor-derived neutrophil extracellular trap-associated DNA impairs treatment efficacy in breast cancer via CCDC25-dependent epithelial-mesenchymal transition.The Journal of clinical investigation · 2026Article
- Plasma Extracellular Vesicles Contain Protein Biomarkers for Capturing Stages of Metabolic Dysfunction-Associated Steatotic Liver Disease: A Preliminary Exploratory Study.Biomolecules · 2025Article
Corrections and comments
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Authors and funding
14 authors.
Funding
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Abstract
The DNA component of neutrophil extracellular traps (NET-DNA) is associated with cancer metastasis and chemotherapy resistance. However, recent studies have suggested that NET-DNA contributes to the activation of dendritic cells (DCs) and promotes the innate immune response to anticancer immunity. Therefore, exploring therapeutic approaches to inhibit NET-mediated tumor progression while maintaining antitumor immunity is essential. Our groups recently identified CCDC25 as a specific NET-DNA sensor on the cytoplasmic membrane of cancer cells that promotes cancer metastasis. In this study, we performed small-molecule compound screening and revealed that mitoxantrone (MTO) could block the interaction between NET-DNA and CCDC25. Molecular docking results indicated that MTO competed with NET-DNA by binding with the amino acid residues Tyr
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