WU Shengnan, JIANG Huanyu, CHEN Haoran, WANG Xinyao, WU Jiahui, WANG Luqi. Differentially expressed genes of ulcerative colitis and associated microRNAs based on bioinformatics analysis[J]. Journal of Clinical Medicine in Practice, 2024, 28(1): 48-55. DOI: 10.7619/jcmp.20233250
Citation: WU Shengnan, JIANG Huanyu, CHEN Haoran, WANG Xinyao, WU Jiahui, WANG Luqi. Differentially expressed genes of ulcerative colitis and associated microRNAs based on bioinformatics analysis[J]. Journal of Clinical Medicine in Practice, 2024, 28(1): 48-55. DOI: 10.7619/jcmp.20233250

Differentially expressed genes of ulcerative colitis and associated microRNAs based on bioinformatics analysis

More Information
  • Received Date: October 12, 2023
  • Revised Date: December 15, 2023
  • Available Online: January 22, 2024
  • Objective 

    To analyze differentially expressed genes and potential microRNA (miRNAs) with diagnostic and therapeutic potential in ulcerative colitis (UC) based on bioinformatics.

    Methods 

    The chip raw data in GEO database was screened by weighted gene coexpression network analysis. UC related differentially expressed genes were obtained for enrichment analysis. Potential miRNAs associated with differentially expressed genes were predicted based on key genes, and gene-miRNA regulatory networks were constructed.

    Results 

    A total of 277 differentially expressed genes were screened, of which 200 genes were up-regulated and 77 genes were down-regulated. Gene set enrichment analysis (GSEA) showed that the main enrichment pathways were neuroactive ligand-receptor interaction, leishmania infection, prion disease and electrocardiogram receptor interaction. The results of gene ontology (GO) analysis showed that it was mainly involved in chemokine activity, heparin binding as well as chemokine receptor binding and other items. The Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed that the main enrichment pathways were cytokine receptor interaction pathway, phosphatidylinositol-3 kinase/protein kinase B(PI3K-AKT) signaling pathway, chemokine signaling pathway as well as nuclear transcription factor kappa B(NF-κB) signaling pathway and other pathway. A total of 10 hub genes were screened: C-X-C chemokine ligand 8 (CXCL8), Toll-like receptor 2 (TLR2), intercellular adhesion molecule-1 (ICAM-1), selectin L (SELL), C-X-C chemokine receptor type 4 (CXCR4), cytotoxic T lymphocyte associated antigen 4 (CTLA4), cluster of differentiation 69 (CD69), and Biglycan (BGN), C-X-C chemokine ligand 13 (CXCL13), tissue inhibitor of metalloproteinases 1(TIMP1). A total of 12 potentially key miRNAs were identified, they were respectively hsa-mir-335-5p, hsa-mir-146a-5p, hsa-mir-92a-3p, hsa-mir-155-5p, hsa-mir-26b-5p, hsa-mir-4426, hsa-mir-4462b, hsa-mir-4647, hsa-mir-32-5p, hsa-mir-92b-3p, hsa-mir-98-5p and hsa-mir-93-5p, respectively.

    Conclusion 

    In this study, a total of 277 differentially expressed genes are screened for possible involvement in the development of UC, and 10 hub genes and 12 miRNAs are identified as possible biomarkers for UC.

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