Upregulation of Long Noncoding Rnas Pacer, Miat, Lincrna-P21, and Lincrna-Cox2 in Ulcerative Colitis As Potential Biomarkers: A Case-Control Study on Their Association With Nf-Кв Activation Publisher Pubmed



Karimpour A ; A ; Zare M ; Jabarpour M ; F ; Panahi G
Source: Medicine (United States) Published:2025

Abstract

Ulcerative colitis (UC), a subtype of inflammatory bowel disease, is characterized by chronic intestinal inflammation. The nuclear factor kappa B (NF-κB) pathway plays a critical role, and long noncoding RNAs (lncRNAs) are emerging as important regulators of gene expression. This study investigated 4 lncRNAs - PACER, myocardial infarction associated transcript (MIAT), lincRNA-p21, and lincRNA-Cox2-in colon tissues of UC patients and healthy controls, exploring their association with NF-κB activation. A total of 35 UC patients and 35 healthy controls were recruited from Shariati Hospital in Tehran, Iran. Real-time qPCR and Western blot measured lncRNA and NF-κB pathway protein levels. Statistical analyses included t-tests/Mann-Whitney U tests for group comparisons, Pearson/Spearman correlations for lncRNA-NF-κB relationships, and receiver operating characteristic analysis for diagnostic potential. PACER, MIAT, lincRNA-p21, and lincRNA-Cox2 were significantly upregulated in UC colon tissues compared to controls (all P ≤ .005). NF-κB p65 (P = .035) and phosphorylated NF-κB p65 (p-NF-κB p65; P = .008) levels were also significantly increased in UC. Expression of all 4 lncRNAs showed significant positive correlation with p-NF-κB p65 levels (all P < .05), suggesting a potential link between these lncRNAs and NF-κB activation in UC. receiver operating characteristic analysis demonstrated good diagnostic potential for these lncRNAs (AUCs > 0.91, all P < .0001) in differentiating UC. This study suggests that PACER, MIAT, lincRNA-p21, and lincRNA-Cox2 are dysregulated in UC and may be associated with NF-κB activation. These lncRNAs may serve as potential diagnostic biomarkers for UC. Further studies are needed to fully elucidate their role in UC pathogenesis and explore their potential as therapeutic targets. This record is sourced from MEDLINE/PubMed, a database of the U.S. National Library of Medicine