Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 116, Issue 11, Pages 2658-2666Publisher
WILEY
DOI: 10.1002/jcb.25214
Keywords
MicroRNA; miR-25; 3T3-L1; ADIPOGENESIS
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Funding
- Croucher Foundation
- National Basic Research Program [2012CB911201]
- National Natural Science Foundation [31171397, 31271533]
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In the past decade, miRNA emerges as a vital player in orchestrating gene regulation and maintaining cellular homeostasis. It is well documented that miRNA influences a variety of biological events, including embryogenesis, cell fate decision, and cellular differentiation. Adipogenesis is an organized process of cellular differentiation by which pre-adipocytes differentiate towards mature adipocytes. It has been shown that adipogenesis is tightly modulated by a number of transcription factors such as PPAR, KLF4, and C/EBP. However, the molecular mechanisms underlying the missing link between miRNA and adipogenesis-related transcription factors remain elusive. In this study, we unveiled that miR-25, a member of miR-106b-25 cluster, was remarkably downregulated during 3T3-L1 adipogenesis. Restored expression of miR-25 significantly impaired 3T3-L1 adipogenesis and downregulated the expression of serial adipogenesis-related genes. Further experiments presented that ectopic expression of miR-25 did not affect cell proliferation and cell cycle progression. Finally, KLF4 and C/EBP, two key regulators of adipocyte differentiation, were experimentally identified as bona fide targets for miR-25. These data indicate that miR-25 is a novel negative regulator of adipocyte differentiation and it suppressed 3T3-L1 adipogenesis by targeting KLF4 and C/EBP, which provides novel insights into the molecular mechanism of miRNA-mediated cellular differentiation. J. Cell. Biochem. 116: 2658-2666, 2015. (c) 2015 Wiley Periodicals, Inc.
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