Investigating the role of lncRNA SNHG14 in early diagnosis and prognosis of acute pancreatitis: a bioinformatics exploration
摘要
Acute pancreatitis (AP) is a severe inflammatory disease. Early and accurate assessment of disease severity remains intricate, highlighting the need for novel biomarkers. Long non-coding RNAs (lncRNAs) play crucial roles in AP pathogenesis.
ObjectiveThis study aimed to investigate the clinical significance and mechanism functional of SNHG14 in AP.
MethodsA prospective cohort of 307 participants (148 AP patients, 159 controls) was recruited. Serum SNHG14 and miR-30a-5p levels were detected by qRT-PCR. An in vitro AP model was established using cerulein (100 nM, 24 h) treatment in AR42J and HPDE6-C7 cells. Functional assays (CCK-8, flow cytometry, ELISA) were performed following SNHG14 knockdown. Bioinformatics analysis was employed for target prediction (starBase, TargetScan, miRDB) and pathway enrichment (KEGG/GO). The SNHG14/miR-30a-5p interaction was confirmed by dual-luciferase assay.
ResultsSNHG14 was significantly up-regulated in AP patients and correlated with disease severity. It showed diagnostic potential for AP (AUC = 0.835) and for identifying severe AP (AUC = 0.757). High SNHG14 level was an independent predictor of poor 28-day prognosis (HR = 4.31, P = 0.018). In vitro, SNHG14 knockdown alleviated cerulein-induced cell apoptosis and secretion of TNF-α, IL-10, and IL-6. SNHG14 functioned as a sponger for miR-30a-5p, and its effects were reversed by miR-30a-5p inhibition. Bioinformatic analysis showed that miR-30a-5p target genes are enriched in autophagy, ubiquitin-mediated proteolysis, and inflammatory pathways.
ConclusionsSNHG14 is a promising biomarker for AP severity and prognosis. The SNHG14/miR-30a-5p axis plays a critical role in regulating inflammation and apoptosis in AP.
SignificanceThis study is the first to delineate the clinical and mechanistic role of the SNHG14/miR-30a-5p axis in AP. It provides a potential candidate for non-invasive RNA-based diagnostic strategies and identifies a potential molecular target for intervention of AP. However, it represents an auxiliary molecular therapy strategies rather than a replacement for existing management.