ArticleFrontiers in immunology2026
Unveiling
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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0 citing papers in PubMed.
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Methods: A systematic experimental strategy was adopted to explore the function of Fusobacterium nucleatum (Fn) in colorectal cancer (CRC) progression. Tissue specimens were collected from healthy volunteers, patients with ulcerative colitis (UC), colorectal adenoma (CRA) and CRC at the First Affiliated Hospital of Henan University of Science and Technology via colonoscopy and surgical resection. Two CRC mouse models, subcutaneous MC38 model and AOM-DSS orthotopic model, were constructed, followed by intratumoral injection or oral gavage of Fn, Streptococcus mutans (S.M.) or normal saline. qPCR was used to quantify Fn abundance in colorectal tissues. IHC and FISH detected inflammatory cytokines and immune cells in tumor tissues. 16S rRNA amplicon sequencing analyzed Fn-mediated alterations in mouse gut microbiota. Flow cytometry and ELISA evaluated immune cell subsets and inflammatory cytokine levels. Western blot examined NLRP3 inflammasome and other proteins expression. Results: In this study, we employed two mouse models of CRC (MC38 subcutaneous and AOM-DSS orthotopic models) to investigate the role of Fn in CRC progression. Our findings demonstrated that Fn administration significantly increased tumor growth compared to controls. Quantitative PCR confirmed elevated Fn abundance in CRC tissues, and microbiome analysis revealed distinct bacterial clades in Fn-treated mice. Immunofluorescence analysis showed enrichment of myeloid cells (CD45/CD11b, CD11C, F4/80,MHCI,MHCII) in tumors, suggesting that Fn reshapes the immune landscape towards a proinflammatory state. Conclusion: Our results establish Fn as a driver of CRC progression through bone marrow-derived immune cell recruitment and NLRP3-dependent inflammatory microenvironment induction. These findings provide new insights into the mechanisms by which Fn contributes to CRC development and suggest potential therapeutic targets for CRC prevention and treatment.
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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.