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Updated: Jan 15, 2026
In vitro Organoid Culture of Primary Mouse Colon Tumors
Published on: May 17, 2013
Downregulation of F11R in Colorectal Cancer and Tumour Progression
Fengjiao Wang1,2, Xiumin Bao1,3,2, Qingchun Lei
1Department of Gastroenterology, Affiliated Hospital of Kunming University of Science and Technology, the First People's Hospital of Yunnan Province, Kunming, China.
Objective:
To evaluate the prognostic value and expression profile of F11R (junctional adhesion molecule-A, JAM-A) in colorectal cancer (CRC) and to elucidate its functional role, particularly in epithelial-mesenchymal transition (EMT) and Rap1 signalling.
Study Design:
Integrated bioinformatic and experimental study. Place and Duration of the Study: Department of Gastroenterology, Affiliated Hospital of Kunming University of Science and Technology, the First People's Hospital of Yunnan Province, Kunming, China, from 1st August 2021 to 30th June 2023.
Methodology:
F11R-associated genes were analysed using The Cancer Genome Atlas (TCGA) and the Human Protein Atlas (HPA). Protein expression was assessed by immunohistochemistry, and cell-type localisation was determined by single-cell RNA-seq. Functional enrichment was performed to explore related pathways. CRC cell proliferation, migration, invasion, and apoptosis were examined with CCK-8, Transwell, scratch, and flow cytometry assays, while EMT-related proteins were evaluated by western blotting.
Results:
F11R expression was significantly reduced in CRC compared with normal tissues. IHC revealed cytoplasmic and membranous localisation, and single-cell data showed enrichment in endothelial and epithelial cells. Enrichment analysis implicated F11R in T-cell receptor signalling, cadherin binding, and tight-junction pathways. Expression correlated with CD4⁺ Th1-like cells, effector and resting Tregs, and effector-memory T cells. Silencing F11R enhanced proliferation, migration, and invasion; reduced apoptosis; and promoted EMT, evidenced by decreased ZO-1 and E-cadherin, increased N-cadherin and vimentin, and Rap1 activation.
Conclusion:
F11R regulates EMT and Rap1 signalling, thereby influencing CRC metastasis. Its reduced expression is associated with unfavourable outcomes and tumour progression. Cell type-specific enrichment in endothelial and epithelial cells, along with links to immune subsets, highlights F11R as a potential prognostic biomarker in CRC.
Key Words:
Colorectal cancer, F11R, Tumour progression, Prognostic potential, Immune infiltration.
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