ArticleMucosal immunology2021
Intestinal epithelium-derived BATF3 promotes colitis-associated colon cancer through facilitating CXCL5-mediated neutrophils recruitment.
Article in Mucosal immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- CXCL5: A coachman to drive cancer progression.Frontiers in oncology · 2022Pooled it
- Succinate drives breast cancer bone metastasis by activating the HIF1α/YTHDF1/YAP signaling axis to upregulate chemokine CXCL5 and disrupt the bone microenvironment.Apoptosis : an international journal on programmed cell death · 2026Article
- CXCL5 is associated with neutrophil-driven intestinal inflammation and IL-17-associated epithelial signaling in inflammatory bowel disease.Scientific reports · 2026Article
- Review
- Functional role of small extrachromosomal circular DNA in colorectal cancer.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Cell cycle dysregulation: a central hub in colitis-associated colorectal carcinogenesis.Frontiers in immunology · 2026Review
- Identification and Validation of BATF3 as a Promising Biomarker Gene for Peripheral T-cell Lymphoma.Current medicinal chemistry · 2026Article
- Integrated multidimensional bioinformatics analysis of the molecular mechanisms of ulcerative colitis-associated colorectal cancer and MMP1 as a potential therapeutic target.Cancer gene therapy · 2025Article
- Transcription factor ELF-1 protects against colitis by maintaining intestinal epithelium homeostasis.Communications biology · 2025Article
- Myeloid-Derived Suppressor Cell Accumulation Drives Intestinal Fibrosis through mCCL6/hCCL15 Chemokine-Mediated Fibroblast Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Neutrophils: From Inflammatory Bowel Disease to Colitis-Associated Colorectal Cancer.Journal of inflammation research · 2025Review
- Review
- Identifying Spatial Co-occurrence in Healthy and InflAmed tissues (ISCHIA).Molecular systems biology · 2024Article
- PLOD3 facilitated T cell activation in the colorectal tumor microenvironment and liver metastasis by the TNF-α/ NF-κB pathway.Journal of translational medicine · 2024Article
- Beyond the horizon: Neutrophils leading the way in the evolution of immunotherapy.Cancer medicine · 2023Review
- Colitis-associated carcinogenesis: crosstalk between tumors, immune cells and gut microbiota.Cell & bioscience · 2023Review
- CXCL5 promotes tumorigenesis and angiogenesis of glioblastoma via JAK-STAT/NF-κb signaling pathways.Molecular biology reports · 2023Article
- m6A modification-mediated BATF2 suppresses metastasis and angiogenesis of tongue squamous cell carcinoma through inhibiting VEGFA.Cell cycle (Georgetown, Tex.) · 2023Article
- miRNA effects on gut homeostasis: therapeutic implications for inflammatory bowel disease.Trends in immunology · 2022Review
- Expression of Autophagic and Inflammatory Markers in Normal Mucosa of Individuals with Colorectal Adenomas: A Cross Sectional Study among Italian Outpatients Undergoing Colonoscopy.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
20 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Inflammation is a critical player in the development and progression of colon cancer. Basic leucine zipper transcription factor ATF-like 3 (BATF3) plays an important role in infection and tumor immunity through regulating the development of conventional type 1 dendritic cells (cDC1s). However, the function of BATF3 in colitis and colitis-associated colon cancer (CAC) remains unclear. Here, BATF3 wild-type and knockout mice were used to construct an AOM/DSS-induced CAC model. In addition, DSS-induced chronic colitis, bone marrow cross-transfusion (BMT), neutrophil knockout, and other animal models were used for in-depth research. We found that BATF3 deficiency in intestinal epithelial cells rather than in cDC1s inhibited CAC, which was depended on inflammatory stimulation. Mechanistically, BATF3 directly promoted transcription of CXCL5 by forming a heterodimer with JunD, and accelerated the recruitment of neutrophils through the CXCL5-CXCR2 axis, ultimately increasing the occurrence and development of CAC. Tissue microarray and TCGA data also indicated that high expression of BATF3 was positively correlated with poor prognosis of colorectal cancer and other inflammation-related tumors. In summary, our results demonstrate that intestinal epithelial-derived BATF3 relies on inflammatory stimulation to promote CAC, and BATF3 is expected to be a novel diagnostic indicator for colitis and CAC.
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