The co-expression of Crohn’s disease and colon cancer network was analyzed by bioinformatics-CXCL1 Tumour microenvironment and prognosis-related gene CXCL1

Author:

Mao Zijuan1,Gu Yuyang2,Dai Qiang3,Tao Ganxue1,Fei Zhenhua1,Xu Yangjie4

Affiliation:

1. The First Affiliated Hospital of Wenzhou Medical University

2. Yuyang Gu, The First Affiliated Hospital of Jiaxing University

3. Rui’an People’s Hospital, The Third Affiliated Hospital of Wenzhou Medical University

4. Yangjie Xu, Wenzhou Medical University

Abstract

Abstract

Purpose This study aimed to investigate the molecular links and mechanisms between Crohn’s disease (CD) and colorectal cancer (CRC). Methods This study used the Gene Expression Omnibus (GEO) database to identify Differentially expressed genes (DEGs) in CD (GSE112366) and CRC (GSE110224), analyzed by 'edgeR' and 'limma'. The Gene Ontology and the Kyoto Encyclopedia of Genes and Genomes explored DEG functions, and the Search Tool for the Retrieval of Interacting Genes (STRING) informed the protein-protein interaction network construction visualized in Cytoscape (version 3.7.2). Cyto-Hubba identified key genes, whose biomarker potential for CD and CRC was evaluated. Results The study discovered 61 DEGs, with 44 up- and 17 down-regulated, linked to immune responses and signaling pathways. CXCL1, highly expressed in colon cancer, correlated with better prognosis and lower staging. It also showed associations with immune infiltration and checkpoint molecules, suggesting a role in cancer progression and retreat. Conclusion CXCL1 may play a role in the development of colorectal cancer from inflammatory bowel disease.

Publisher

Springer Science and Business Media LLC

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4. Bule P, Aguiar SI, Aires-Da-Silva F, Nunes Ribeiro J. Dias. 2021. ‘Chemokine-Directed Tumour Microenvironment Modulation in Cancer Immunotherapy’. International Journal of Molecular Sciences 22 (18): 9804. https://doi.org/10.3390/ijms22189804.

5. ‘CXCL1 Derived from Tumour-Associated Macrophages Promotes Breast Cancer Metastasis via Activating NF-κB/SOX4 Signaling - PubMed’. n.d. Accessed 10. June 2023. https://pubmed.ncbi.nlm.nih.gov/30158589/.

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