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.

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.