Investigating the role of lncRNA SNHG14 in early diagnosis and prognosis of acute pancreatitis: a bioinformatics exploration

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. This study aimed to investigate the clinical significance and mechanism functional of SNHG14 in AP. A 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. SNHG14 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. SNHG14 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. This 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.