ArticleCentral-European journal of immunology2025
Predictive value of long non-coding RNA DDX11-AS1 in inflammatory bowel disease and its effect on intestinal mucosal cell function.
Article in Central-European journal of immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
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Authors and funding
4 authors.
Funding
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Abstract
Introduction: Inflammatory bowel disease (IBD) is a chronic and recurrent autoimmune condition. Numerous studies have reported that non-coding RNA, especially long non-coding RNA (lncRNA), plays a significant role in the regulation of IBD. This study sought to investigate the expression of lncRNA DDX11-antisense RNA 1 (DDX11-AS1) in IBD and its potential diagnostic value, while also evaluating the influence of DDX11-AS1 on the functionality of colorectal mucosal cells. Material and methods: The expression trend of DDX11-AS1 was determined through PCR analysis, with its clinical diagnostic value assessed via ROC curve analysis. To construct an in vitro inflammation cell model, a commercially available human normal colon epithelial cell line (FHC) was selected and induced with lipopolysaccharide (LPS). Subsequently, the CCK-8 kit, flow cytometry, and ELISA were employed to assess cell viability, apoptosis, and inflammatory responses. The target gene miR-2355-5p of DDX11-AS1 was predicted using the Encyclopedia of RNA Interactomes (ENCORI), and the interaction relationship was validated by luciferase reporting assays. Results: The study found that DDX11-AS1 expression is elevated, while miR-2355-5p expression is decreased, in patients with IBD. DDX11-AS1 demonstrated high diagnostic accuracy for IBD. In vitro, LPS exposure stimulated inflammation and apoptosis, and reduced cell viability in FHC cells. Downregulating DDX11-AS1 mitigated LPS-induced damage in these cells. Mechanistically, DDX11-AS1 was shown to directly target miR-2355-5p, exhibiting an inverse relationship. Conclusions: The study findings suggest that the upregulation of DDX11-AS1 contributes to LPS- induced apoptosis and inflammation by targeting miR-2355-5p, offering new insights into the pathogenesis of IBD.
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