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Persistent Gene Activation as a Molecular Signature of Ulcerative Colitis Progression to Colorectal Cancer
Yuxiao Ji1, Pengchong Li1, Yuqi Liu2
1Department of Gastroenterology, Beijing Friendship Hospital, Capital Medical University, National Clinical Research Center for Digestive Disease, Beijing Digestive Disease Center, State Key Laboratory of Digestive Health, 95 Yong'an Road, Xicheng District, Beijing, 100050, China.
Digestive Diseases and Sciences
|February 19, 2026
Summary
Seven genes are consistently elevated in ulcerative colitis (UC) and colitis-associated colorectal cancer (CAC) progression. Upregulated PD-L1 in neutrophils suggests immune suppression, highlighting potential biomarkers for early cancer detection and treatment.
Area of Science:
- Gastroenterology
- Oncology
- Immunology
Background:
- Ulcerative colitis (UC) involves colonic epithelial damage and carries an increased risk of malignant transformation over time.
- Mechanisms linking chronic inflammation in UC to colorectal cancer (CAC) development are not fully understood.
Purpose of the Study:
- Identify genes contributing to the transition from healthy controls (HC) to UC and subsequently to CAC.
- Investigate the role of neutrophils and immune pathways in UC-related tumorigenesis.
Main Methods:
- Bioinformatic analysis of Gene Expression Omnibus (GEO) datasets to identify differentially expressed genes.
- Functional enrichment and immune infiltration analyses.
- In vitro experiments assessing Programmed Death-Ligand 1 (PD-L1) expression in neutrophils stimulated with Interferon-gamma (IFN-γ) and Tumor Necrosis Factor-alpha (TNF-α).
Main Results:
- Seven genes (S100A8, IL33, MGP, MMP3, CFI, CLU, CLEC4E) were upregulated in both HC to UC and UC to CAC transitions.
- These genes are associated with neutrophils and pathways including IFN-γ, TNF-α, and oxidative phosphorylation.
- IFN-γ and TNF-α stimulation significantly increased PD-L1 expression in neutrophils.
Conclusions:
- Seven genes are persistently upregulated during UC and CAC progression, influencing neutrophils and inflammatory/tumorigenic pathways.
- Increased PD-L1 on neutrophils suggests a role for neutrophil-mediated immune suppression in CAC progression.
- These genes and PD-L1 represent potential molecular markers and therapeutic targets for early intervention in UC-related cancer.
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