{"title":"F11R在结直肠癌和肿瘤进展中的下调","authors":"Fengjiao Wang, Xiumin Bao, Qingchun Lei, Xiao Yuan, Xiaodan Tang, Pengli Zhang","doi":"10.29271/jcpsp.2025.10.1269","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>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.</p><p><strong>Study design: </strong>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.</p><p><strong>Methodology: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p><p><strong>Key words: </strong>Colorectal cancer, F11R, Tumour progression, Prognostic potential, Immune infiltration.</p>","PeriodicalId":94116,"journal":{"name":"Journal of the College of Physicians and Surgeons--Pakistan : JCPSP","volume":"35 10","pages":"1269-1278"},"PeriodicalIF":0.8000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Downregulation of F11R in Colorectal Cancer and Tumour Progression.\",\"authors\":\"Fengjiao Wang, Xiumin Bao, Qingchun Lei, Xiao Yuan, Xiaodan Tang, Pengli Zhang\",\"doi\":\"10.29271/jcpsp.2025.10.1269\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>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.</p><p><strong>Study design: </strong>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.</p><p><strong>Methodology: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>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.</p><p><strong>Key words: </strong>Colorectal cancer, F11R, Tumour progression, Prognostic potential, Immune infiltration.</p>\",\"PeriodicalId\":94116,\"journal\":{\"name\":\"Journal of the College of Physicians and Surgeons--Pakistan : JCPSP\",\"volume\":\"35 10\",\"pages\":\"1269-1278\"},\"PeriodicalIF\":0.8000,\"publicationDate\":\"2025-10-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of the College of Physicians and Surgeons--Pakistan : JCPSP\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.29271/jcpsp.2025.10.1269\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of the College of Physicians and Surgeons--Pakistan : JCPSP","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.29271/jcpsp.2025.10.1269","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Downregulation of F11R in Colorectal Cancer and Tumour Progression.
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.
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