Glucose-induced microRNA-17 promotes pancreatic beta cell proliferation through down-regulation of Menin.

OBJECTIVE Menin, encoded by the Men1 gene, is responsible for β-cell tumor formation in patients with multiple endocrine neoplasia type 1. Recently, Menin has been proven to negatively regulate β-cell proliferation in several mouse models, including hyperglycemia. However, it is unclear how glucose regulates Menin expression in β-cells. MATERIALS AND METHODS In the present study, quantitative real-time reverse transcriptase-polymerase chain reaction analysis was performed to detect the expression levels of MicroRNAs in Min-6 cells treated with high glucose, in which we found that miR-17 was significantly up-regulated. RESULTS Further studies using bioinformatic prediction, luciferase and protein expression analysis suggested that miR-17 could inhibit protein levels of Menin through targeting its 3'-untranslated region. CONCLUSIONS Our results indicate that miR-17 might serve as an important intracellular target of glucose to mediate the mitogenic effect that glucose exerts in pancreatic β-cells.