ArticleImmunity, inflammation and disease2024
Knockdown of TOP2A suppresses IL-17 signaling pathway and alleviates the progression of ulcerative colitis.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 8 citations in OpenAlex.
- CXCL5 is associated with neutrophil-driven intestinal inflammation and IL-17-associated epithelial signaling in inflammatory bowel disease.Scientific reports · 2026Article
- A dual-functional Janus nanofibrous membrane as an immunomodulatory barrier for periodontitis regeneration under diabetic conditions.Materials today. Bio · 2026Article
- Mechanism of Artemisia argyi Levl.et Vant. aqueous extract in alleviating dextran sulfate sodium-induced ulcerative colitis.Scientific reports · 2025Article
- TOP2A Promotes Proliferation, Migration, and Inflammatory Response in M5-Treated Keratinocytes by Binding CTBP1 to Activate Wnt/β-Catenin Signaling.Cell biochemistry and biophysics · 2025Article
- Targeting the IL-23 Receptor Gene: A Promising Approach in Inflammatory Bowel Disease Treatment.International journal of molecular sciences · 2025Review
- Article
- Knockdown of TOP2A suppresses IL-17 signaling pathway and alleviates the progression of ulcerative colitis.Immunity, inflammation and disease · 2024Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundUlcerative colitis (UC) is a chronic inflammatory disease of the colonic mucosa, with a gradually increasing incidence. Therefore, it is necessary to actively seek targets for the treatment of UC.
methodsCommon differentially expressed genes (DEGs) were screened from two microarray data sets related to UC. Protein-protein interaction network was constructed to find the hub genes. The UC mouse model and cell model were induced by dextran sulfate sodium (DSS). The pathological changes of colon tissue were observed by hematoxylin-eosin staining. Immunohistochemistry and immunofluorescence were performed to detect the expressions of Ki67 and Claudin-1. The performance of mice was observed by disease activity index (DAI). The effect of TOP2A on proliferation, inflammation, oxidative stress, and interleukin-17 (IL-17) signaling pathway in UC model was measured by cell counting kit-8, enzyme-linked immunosorbent assay, and western blot.
resultsThrough bioinformatics analysis, 295 common DEGs were screened, and the hub gene TOP2A was selected. In UC model, there was obvious inflammatory cell infiltration in the colon and less goblet cells, while si-TOP2A lessened it. More Ki67 positive cells and less Claudin-1 positive cells were observed in UC model mice. Furthermore, knockdown of TOP2A increased the body weight and colon length of UC mice, while the DAI was decreased. Through in vivo and in vitro experiments, knockdown of TOP2A also inhibited inflammation and IL-17 signaling pathway, and promoted proliferation in DSS-induced NCM460 cells.
conclusionKnockdown of TOP2A alleviated the progression of UC by suppressing inflammation and inhibited IL-17 signaling pathway.
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