Evidence map›Paper›PMID 39656543›Full record

ArticleThe Journal of clinical investigation2025

Fusobacterium nucleatum promotes colorectal cancer through neogenesis of tumor stem cells.

Qinying Wang, Tingting Hu, Qinyuan Zhang, Yichi Zhang, Xiaoxu Dong, Yutao Jin, Jinming Li, Yangyang Guo, Fanying Guo, Ziying Chen and 3 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed.

  1. Review
  2. Article
  3. Journal for immunotherapy of cancer · 2026
    Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Pathogenic Roles ofPathogens (Basel, Switzerland) · 2026
    Review
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Qinying WangDepartment of Colorectal Surgery and.
Tingting HuDepartment of Colorectal Surgery and.
Qinyuan ZhangDepartment of Colorectal Surgery and.
Yichi ZhangDepartment of Colorectal Surgery and.
Xiaoxu DongDepartment of Colorectal Surgery and.
Yutao JinDepartment of Colorectal Surgery and.
Jinming LiDepartment of Colorectal Surgery and.
Yangyang GuoDepartment of Colorectal Surgery and.
Fanying GuoDepartment of Colorectal Surgery and.
Ziying ChenDepartment of Colorectal Surgery and.
Peijie ZhongDepartment of Colorectal Surgery and.
Yongzhi YangDepartment of Colorectal Surgery and.
Yanlei MaDepartment of Colorectal Surgery and.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intestinal stem cells are crucial for maintaining intestinal homeostasis, yet their transformation into tumor stem cells in the context of microbial infection remains poorly understood. Fusobacterium nucleatum is frequently associated with the onset and progression of colorectal cancer (CRC). In this study, we uncovered that F. nucleatum colonized the depths of gut crypts in both patients with CRC and mouse models. Through single-cell sequencing analysis, we demonstrated that F. nucleatum infection reprogrammed crypt cells and activated lymphocyte antigen 6 complex, locus A+ ( LY6A+, also known as stem cell antigen 1 [Sca-1]) revival stem cells (RSCs), promoting their hyperproliferation and subsequent transformation into tumor stem cells, which accelerated intestinal carcinogenesis. Mechanistically, we identified LY6A as a glycosylphosphatidylinositol-anchored (GPI-anchored) membrane receptor for F. nucleatum. Upon binding, F. nucleatum induced the upregulation of ribosomal protein S14 (RPS14) via the LY6A receptor, driving RSC hyperactivity and tumorigenic conversion. Functional studies showed that genetic ablation of Ly6a in intestinal epithelial cells or Rps14 in LY6A+ RSCs substantially reduced F. nucleatum colonization and tumorigenesis. Moreover, analysis of clinical CRC cohorts revealed a strong correlation between F. nucleatum infection, RSC expansion, and elevated RPS14 expression in tumor tissues. These findings highlight an alternative F. nucleatum/LY6A/RPS14 signaling axis as a critical driver of CRC progression and propose potential therapeutic targets for effective CRC intervention.

Indexed as

Colorectal NeoplasmsFusobacterium InfectionsFusobacterium nucleatumNeoplasm ProteinsNeoplastic Stem CellsAnimalsAntigens, LyCarcinogenesisFemaleHumansMaleMembrane ProteinsMiceRibosomal ProteinsAntigens, LyLy6a protein, mouseMembrane ProteinsNeoplasm ProteinsRibosomal ProteinsBacterial infectionsCancerColorectal cancerGastroenterologyOncology

Identifiers

PMID39656543
PMCPMC11785920

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Registered trials

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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.