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Cell Signal. 2014 Nov;26(11):2583-9. doi: 10.1016/j.cellsig.2014.07.017. Epub 2014 Jul 16.

miR-709 inhibits 3T3-L1 cell differentiation by targeting GSK3β of Wnt/β-catenin signaling.

Author information

  • 1State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou 510006, PR China.
  • 2State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou 510006, PR China. Electronic address: chyaosh@mail.sysu.edu.cn.

Abstract

Adipocyte differentiation is tightly regulated by altering gene expression in which microRNAs might be strong post-transcriptional regulators. In this study, we examined the roles of miR-709 in adipogenic differentiation of 3T3-L1 preadipocyte. We found that miR-709 expression was down-regulated during adipogenesis after MDI (1-methyl-3-isobutylxanthine, dexamethasone and insulin) stimulation in normal cultured 3T3-L1 cells, while up-regulated after LiCl treatment. Overexpression of miR-709 inhibited adipogenic differentiation of 3T3-L1 cells. We demonstrated that miR-709 directly targeted 3' UTR of GSK3β (glycogen synthase kinase 3 beta). Overexpression of miR-709 decreased GSK3β protein but not mRNA level. Furthermore, the inhibition of miR-709 could be counteracted by overexpression of GSK3β during 3T3-L1 adipogenic differentiation. In addition, miR-709 increased both protein and mRNA levels of β-catenin, which is the downstream effector of GSK3β in Wnt/β-catenin signaling pathway, and subsequently elevated the expression of target of β-catenin which represses adipogenesis. These data indicate that miR-709 inhibits adipocyte differentiation through targeting GSK3β and subsequently activating Wnt/β-catenin signaling pathway.

Copyright © 2014 Elsevier Inc. All rights reserved.

KEYWORDS:

Adipogenesis; GSK3β; miR-709; β-Catenin signaling

PMID:
25038456
[PubMed - in process]
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