Knocking down clock control gene CRY1 decreases adipogenesis via canonical Wnt/β-catenin signaling pathway
Cryptochrome gene 1(CRY1) is a member of circadian clock genes, which play an important role in adipocyte biology. CRY1 was reported to be related with the lipid metabolism, but the molecule mechanism of CRY1 in regulating the adipogenesis remains unclear. Here we report that CRY1 is a key regulator...
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Published in | Biochemical and biophysical research communications Vol. 506; no. 3; pp. 746 - 753 |
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Main Authors | , , , , |
Format | Journal Article |
Language | English |
Published |
United States
Elsevier Inc
30.11.2018
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Subjects | |
Online Access | Get full text |
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Summary: | Cryptochrome gene 1(CRY1) is a member of circadian clock genes, which play an important role in adipocyte biology. CRY1 was reported to be related with the lipid metabolism, but the molecule mechanism of CRY1 in regulating the adipogenesis remains unclear. Here we report that CRY1 is a key regulator in adipogenic differentiation. We found that the expression levels of CRY1 in 3T3-L1 cells and C3H10T1/2 cells gradually increased during the process of adipogenic differentiation. Knockdown of endogenous CRY1 significantly inhibited the expression of adipogenic markers and lipid droplet formation in cells under adipogenic induction. In addition, knockdown of endogenous CRY1 promoted the expression and nuclear accumulation of β-catenin, the critical signal molecular in the canonical canonical Wnt signaling pathway, suggesting the regulation effect of CRY1 in adipogenesis was mediated by canonical Wnt/β-catenin signaling. Taken together, our study suggests that CRY1 regulates adipogenic differentiation through modulating the canonical Wnt/β-catenin signaling pathway.
•Adipogenic differentiation induces CRY1 expression.
.•Knockdown of CRY1 inhibits adipogenic differentiation and adipogenesis-specific gene expression.•Knockdown of CRY1 activates canonical Wnt/β-catenin signaling pathway. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2018.10.134 |