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

Y Lu1, X-Q Fei, S-F Yang

  • 1Department of Endocrinology, Taizhou People's Hospital, Nantong University, Taizhou, Jiangsu, China. luyu_666@126.com.

European Review for Medical and Pharmacological Sciences
|March 11, 2015
PubMed
Abstract

Insights

High glucose increases miR-17 in pancreatic beta cells, which then inhibits Menin protein. This pathway explains how glucose promotes beta cell proliferation.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Cell Biology

Background:

  • Menin, encoded by the Men1 gene, is implicated in pancreatic beta-cell tumor formation and negatively regulates beta-cell proliferation.
  • The precise mechanisms by which glucose influences Menin expression in beta-cells remain largely unelucidated.

Purpose of the Study:

  • To investigate the regulatory role of glucose on Menin expression in pancreatic beta-cells.
  • To identify potential microRNAs (miRNAs) involved in glucose-mediated Menin regulation.

Main Methods:

  • Quantitative real-time reverse transcriptase-polymerase chain reaction (qRT-PCR) was employed to assess miRNA expression in Min-6 cells exposed to high glucose.
  • Bioinformatic prediction, luciferase assays, and Western blotting were utilized to validate the interaction between miR-17 and Menin.

Main Results:

  • High glucose significantly upregulated miR-17 expression in Min-6 cells.
  • miR-17 was found to directly target the 3'-untranslated region of Menin mRNA, leading to inhibition of Menin protein levels.

Conclusions:

  • miR-17 acts as a key intracellular mediator of glucose's mitogenic effects on pancreatic beta-cells.
  • The glucose-miR-17-Menin axis represents a novel regulatory pathway in beta-cell proliferation and potentially in the pathogenesis of related tumors.

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