miR‑92a‑3p regulates trypsinogen activation via Egr1 in AR42J cells

Acute pancreatitis (AP) exhibits high morbidity and mortality rates. The onset of AP is characterized by early trypsinogen activation.The present study aimed to investigate the expression of microRNA (miR)‑92a‑3p and early growth response protein 1 (Egr1), and the effect of miR‑92a‑3p on trypsinogen activation in the pancreatic exocrine cell line AR42J. mRNA and miRNA microarrays were used to identify differentially expressed mRNAs and miRNAs in AR42J cells. A miRNA‑mRNA network was constructed using bioinformatics software, and Egr1 and its regulated miRNA subnetworks were identified by reviewing previous literature. The results suggested that miR‑92a‑3p could bind to Egr1 3'untranslated region sequence. Subsequently, miR‑92a‑3p mimic and inhibitor were used to transfect AR42J cells. Following transfection, reverse transcription‑quantitative PCR and western blotting were performed to detect Egr1 expression. Furthermore, AR42J cells were cotransfected with miR‑92a‑3p inhibitor and small interfering (si)‑Egr1. The trypsinogen activation rate of AR42J cells was measured by flow cytometry. Microarrays and bioinformatics results indicated that Egr1 may be a target gene of miR‑92a‑3p. In addition, the present study suggested that miR‑92a‑3p downregulated Egr1 in vitro and that miR‑92a‑3p and Egr1 expression was associated with trypsinogen activation. Furthermore, miR‑92a‑3p inhibitor reversed the effect of si‑Egr1 on trypsinogen activation. In conclusion, miR‑92a‑3p may negatively regulate the activation of trypsinogen in AR42J cells via Egr1.