Predictive value of long non-coding RNA DDX11-AS1 in inflammatory bowel disease and its effect on intestinal mucosal cell function.

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.