ArticleNature communications2025
Agonist signaling drives neutrophil subpopulations to promote/inhibit colorectal cancer liver metastasis.
Article in Nature communications, 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Neutrophil extracellular traps in colorectal cancer: context-dependent roles from inflammatory carcinogenesis to liver metastasis and therapeutic targeting.Journal of translational medicine · 2026Review
- Interactions Between Circulating Tumor Cells and the Immune System in Colorectal Cancer: Friends or Foes?Cancers · 2026Review
- Nucleotide signaling in neutrophils: a key player in cancer dynamics.Purinergic signalling · 2026Review
- Review
- Myeloid-derived suppressor cells in colorectal cancer: mechanisms of immunosuppression, therapy resistance and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Review
- Advances in the study of low-density neutrophils in rheumatic diseases.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
Liver metastasis is a primary cause of death in colorectal cancer, yet the role of immune cells called neutrophils in this process remains complex. In this study, we identify three distinct neutrophil subtypes: anti-tumor high-density neutrophils, pro-tumor mature low-density neutrophils, and immature low-density neutrophils. Here we show that tumor-derived GM-CSF converts anti-tumor neutrophils into a pro-tumor state via the AKT-NF-κB-NFAT5 signaling axis. These activated neutrophils, when further stimulated by CXCR2 ligands, release web-like structures known as neutrophil extracellular traps which promote cancer spread by enhancing cancer cell growth, suppressing immune responses, and preparing the liver for metastasis. Importantly, we demonstrate that using antibodies depleting neutrophils or drugs inhibiting their pro-tumor activity effectively reduces liver metastasis in mice. Our work defines specific neutrophil subsets as key drivers of cancer progression and highlights their therapeutic potential in preventing metastatic spread.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.