Clinical Significance of miR-3619-5p Expression in Patients with Type 2 Diabetes and Its Regulation of Pancreatic β-Cell Proliferation

The core pathological feature of type 2 diabetes mellitus (T2DM) is pancreatic β-cell failure; therefore, the identification of effective circulating biomarkers and molecular targets that regulate pancreatic β-cell homeostasis is of significant practical importance. As key regulatory molecules of gene expression, miRNAs play an important role in the proliferation, apoptosis, and insulin secretion of pancreatic β-cells. The purpose of this study is to investigate the expression patterns and clinical value of miR-3619-5p in the serum of T2DM and to clarify its regulatory role in pancreatic β-cell proliferation. RT-qPCR was used to detect the expression of miR-3619-5p and MTA3. ROC curves were used to evaluate diagnostic performance. Bioinformatics and dual-luciferase assays were used to validate the target-ligand relationship. Cell proliferation was measured by CCK-8 assay, while apoptosis was examined via flow cytometry. Insulin secretion levels were measured using ELISA. The results showed that miR-3619-5p and MTA3 were downregulated in T2DM patients and pancreatic β-cells. miR-3619-5p might be a biomarker for the diagnosis of T2DM; its overexpression promotes cell proliferation, inhibits apoptosis, and enhances insulin secretion. miR-3619-5p targets and regulates MTA3, and the two are significantly positively correlated. miR-3619-5p mimic can reverse the damage caused by si-MTA3 to pancreatic β-cell function. In short, miR-3619-5p is downregulated in T2DM and has diagnostic value. miR-3619-5p may participate in the regulation of pancreatic β-cell function by targeting MTA3.