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Updated: Mar 29, 2026

Investigating Target Gene Function in a CD40 Agonistic Antibody-induced Colitis Model using CRISPR/Cas9-based Technologies
Published on: June 2, 2021
Bioinformatic analysis of potential candidates for therapy of inflammatory bowel disease
1Pharmacy Department, China-Japan Union Hospital of Jilin University, Changchun, China. changyuzhoucyz@163.com.
Objective:
Inflammatory bowel diseases (IBDs) including ulcerative colitis (UC) and Crohn's disease (CD) increased the risk for developing colorectal cancer. However, there is no effective therapy for IBDs. The aim of this study was to identify potential therapeutic targets for inflammatory bowel disease (IBD) and explore the possible mechanism underlying this disease.
Materials And Methods:
Gene expression profile GSE6731 was downloaded from Gene Expression Omnibus database, which included 9 UC samples and 19 CD samples. Differentially expressed genes (DEGs) between affected colon tissues and non-affected tissues were identified in UC and CD group. Then, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis of DEGs were performed. Modules in the protein-protein interaction (PPI) network were identified, and significant node genes were selected.
Results:
Total 619 DEGs including 285 up-regulated genes and 334 down-regulated genes were identified in UC group and total 1159 DEGs of CD including 585 up-regulated genes and 574 down-regulated genes were selected. Module was selected from PPI network. From the PPI network and module, DEGs of mitogen-activated protein kinase 3 (MAPK3), N-myc downstream regulated 1 (NDRG1) and major histocompatibility complex, class II, DR alpha (HLA-DRA) have high degree.
Conclusions:
MAPK3, NDRG1 and HLA-DRA may play key roles in the progression and development of IBD. They may be used as specific therapeutic targets in the treatment of IBD. However, further experiments are still needed to confirm our results.
Insights
Inflammatory bowel diseases (IBDs) increase colorectal cancer risk. This study identifies MAPK3, NDRG1, and HLA-DRA as potential therapeutic targets for IBD treatment.
Area of Science:
- Gastroenterology and Immunology
- Molecular Biology
- Bioinformatics
Background:
- Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn's disease (CD), are chronic conditions associated with an increased risk of colorectal cancer.
- Current therapeutic options for IBDs are limited, highlighting the urgent need for novel treatment strategies.
- Understanding the molecular mechanisms underlying IBD pathogenesis is crucial for identifying effective therapeutic targets.
Purpose of the Study:
- To identify potential therapeutic targets for inflammatory bowel disease (IBD).
- To explore the underlying molecular mechanisms contributing to the development of IBD.
- To analyze gene expression profiles and protein-protein interaction networks in IBD.
Main Methods:
- Downloaded gene expression profile GSE6731 from the Gene Expression Omnibus (GEO) database, comprising 9 UC and 19 CD samples.
- Identified differentially expressed genes (DEGs) between affected and non-affected colon tissues in UC and CD groups.
- Performed Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses, and constructed protein-protein interaction (PPI) networks to identify key genes and modules.
Main Results:
- Identified 619 DEGs in UC (285 up-regulated, 334 down-regulated) and 1159 DEGs in CD (585 up-regulated, 574 down-regulated).
- Selected a significant module from the PPI network.
- Highlighted mitogen-activated protein kinase 3 (MAPK3), N-myc downstream regulated 1 (NDRG1), and major histocompatibility complex, class II, DR alpha (HLA-DRA) as high-degree nodes within the PPI network and module.
Conclusions:
- MAPK3, NDRG1, and HLA-DRA are implicated as key players in the progression and development of IBD.
- These identified genes represent potential specific therapeutic targets for IBD treatment.
- Further experimental validation is required to confirm the role of these genes and their therapeutic potential in IBD.
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