miR-126-3p serves as a biomarker of inflammatory bowel disease (IBD) and modulates the molecular mechanisms of IBD through regulation of DICER1.

BACKGROUND

Inflammatory bowel disease (IBD) imposes a dual burden, physiological and psychological, on patients. This study focused on miR-126-3p to explore its role in the progression of IBD and its potential clinical value.

METHODS

Patients with IBD (including 45 ulcerative colitis [UC] and 36 Crohn's disease [CD]) and controls (50) were enrolled, and clinical data were collected. RT-qPCR was used to quantify miR-126-3p and DICER1 expression. ROC curve analysis was used to assess the diagnostic value of miR-126-3p. Pearson analysis was used to evaluate the associations between miR-126-3p and inflammatory markers (CRP, ESR, TNF-α, IFN-γ) and disease activity scores. In vitro IBD models were established by treating the HT-29 cells with DSS and IEC-6 cells with LPS. Bioinformatics approaches and luciferase reporter assays confirmed that miR-126-3p targets DICER1. Cell viability was assessed using the CCK-8 assay. ELISA was used to quantify inflammatory cytokines across groups.

RESULTS

miR-126-3p was upregulated in UC and CD patients, and correlated with inflammatory markers and disease activity, showing strong ability to distinguish patients from healthy individuals. miR-126-3p targeted DICER1. Downregulation of miR-126-3p reduced the production of proinflammatory factors and ROS induced by DSS or LPS, while silencing DICER1 partially attenuated the protective effect of miR-126-3p inhibition.

CONCLUSION

miR-126-3p is a promising biomarker for IBD diagnosis and assessment of disease activity. The miR-126-3p/DICER1 axis is involved in IBD pathophysiology, suggesting that modulating this axis may provide a therapeutic intervention for IBD.