miR-24 regulates menin in the endocrine pancreas.
نویسندگان
چکیده
Menin, the product of the MEN1 gene, functions as a tumor suppressor and was first identified in 1997 due to its causative role in the endocrine tumor disorder multiple endocrine neoplasia, type 1 (MEN1). More recently, menin has been identified as a key player in pancreatic islet biology with the observation of an inverse relationship between menin levels and pancreatic islet proliferation. However, the factors regulating menin and the MEN1 gene in the pancreas are poorly understood. Here, we describe the regulation of menin by miR-24 and demonstrate that miR-24 directly decreases menin levels and impacts downstream cell cycle inhibitors in MIN6 insulinoma cells and in βlox5 immortalized β-cells. This regulation of menin impacts cell viability and proliferation in βlox5 cells. Furthermore, our data show a feedback regulation between miR-24 and menin that is present in the pancreas, suggesting that miR-24 regulates menin levels in the pancreatic islet.
منابع مشابه
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...
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ورودعنوان ژورنال:
- American journal of physiology. Endocrinology and metabolism
دوره 307 1 شماره
صفحات -
تاریخ انتشار 2014