ArticleJournal for immunotherapy of cancer2025
Neutrophil extracellular traps-STC1 positive feedback loop promotes immune evasion and metastasis in bladder cancer.
Article in Journal for immunotherapy of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed.
- Neutrophil Extracellular Traps in the Tumor Microenvironment: Mechanisms, Immune Regulation, and Implications for Immune Checkpoint Inhibitor Therapy.International journal of molecular sciences · 2026Review
- Multi-omics-driven precision medicine.iMeta · 2026Review
- Immune response to DNA and RNA: structural insights, molecular mechanisms, and therapeutic targeting.Molecular biomedicine · 2026Review
- Review
- Roles of neutrophil extracellular traps in cancer immunotherapy resistance and therapeutic targeting.Biomarker research · 2026Review
- Article
- Metabolic immune checkpoints in cancer: how tumor-derived metabolites shape immunotherapy resistance.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundImmune checkpoint inhibitors (ICIs) have transformed the treatment strategy for bladder cancer (BLCA), but primary resistance still occurs in most patients. Recent evidence suggests that neutrophil extracellular traps (NETs) play a key role in cancer therapy resistance, but their specific role in BLCA remains unclear.
methodsAn integrated analysis of multiple clinical cohorts receiving ICIs was performed to explore the link between NETs and patient outcomes. Immunofluorescence staining, in vitro co-culture system, scanning electron microscopy, and mouse lung metastasis model were used to evaluate the biological effects of NETs. Proteomics and single-cell transcriptomics analysis were further applied to elucidate the molecular mechanisms.
resultsClinically, NETs abnormally accumulated in BLCA and promoted tumor metastasis and immunotherapy resistance in mice. Mechanistically, NETs upregulated the anti-phagocytic checkpoint STC1 in tumor cells through the TLR2-MAPK-FosL1 axis. Notably, STC1 inhibited antigen presentation by sequestering calreticulin, while its secreted form enhances NET formation, forming a self-reinforcing feedback loop. In addition, secreted STC1 impaired differentiation of CD14
conclusionThis study revealed the critical role of the NETs-STC1 feedback loop in BLCA immunoresistance. Targeting this axis could simultaneously enhance efficacy and safety of immunotherapy, providing a novel translational strategy for overcoming resistance in clinical settings.
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