Sulforaphane inhibits mitotic clonal expansion during adipogenesis through cell cycle arrest
Choi KM, Lee YS, Sin DM, Lee S, Lee MK, Lee YM, Hong JT, Yun YP, Yoo HS
Obesity (Silver Spring, Md.) · 72 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- University or hospital
- Chungbuk National University
Based on 1 listed funder(s).
Publication
- Published
- 2012-01-26 · Obesity (Silver Spring) · vol. 20 · issue 7 · pp. 1365–1371
- Publisher
- Wiley
- Cited
- 95 citations · more than 91% of similar papers · 2.8× the field average
- Impact
- Top 10% most cited in its field
- References
- 42 works
- Access
- Free to read
- Research areas
- Genomics, phytochemicals, and oxidative stress · Retinoids in leukemia and cellular processes · Immune Cell Function and Interaction
- Keywords
- Sulforaphane, Adipogenesis, Adipocyte, Internal medicine, Endocrinology, Chemistry, Cell cycle, Biology, Cell biology, Cell, Biochemistry, Medicine, Adipose tissue
- MeSH
- cell line, 3t3-l1 cells, adipocytes, animals, humans, mice, rats, thiocyanates, isothiocyanates, sulfoxides, proliferating cell nuclear antigen, ppar gamma, transcription factors, anticarcinogenic agents, blotting, western, mitosis, cell differentiation, cell proliferation, up-regulation, adipogenesis, cell cycle checkpoints
9 authors
From KR
- Kyeong‐Mi ChoiChungbuk National University
- Youn‐Sun LeeChungbuk National University
- Dong‐Mi SinChungbuk National University
- Seunghyun LeeChungbuk National University
- Mi Kyeong LeeChungbuk National University
- Yong‐Moon LeeChungbuk National University
Abstract
Obesity is a risk factor for numerous metabolic disorders such as type 2 diabetes, hypertension, and coronary heart disease. Adipocyte differentiation is triggered by adipocyte hyperplasia, which leads to obesity. In this study, the inhibitory effect of sulforaphane, an isothiocyanate, on adipogenesis in 3T3-L1 cells was investigated. Sulforaphane decreased the accumulation of lipid droplets stained with Oil Red O and inhibited the elevation of triglycerides in the adipocytes (half-maximal inhibitory concentration = 7.3 µmol/l). The expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer-binding protein α (C/EBPα), major transcription factors for adipocyte differentiation, was significantly reduced by sulforaphane. The major effects of sulforaphane on the inhibition of adipocyte differentiation occurred during the early stage of adipogenesis. Thus, the expression of C/EBPβ, an early-stage biomarker of adipogenesis, decreased in a concentration-dependent manner when the adipocytes were exposed to sulforaphane (0, 5, 10, and 20 µmol/l). The proliferation of adipocytes treated with 20 µmol/l sulforaphane for 24 and 48 h was also suppressed. These results indicate that sulforaphane may specifically affect mitotic clonal expansion to inhibit adipocyte differentiation. Sulforaphane arrested the cell cycle at the G(0)/G(1) phase, increased p27 expression, and decreased retinoblastoma (Rb) phosphorylation. Additionally, sulforaphane modestly decreased the phosphorylation of ERK1/2 and Akt. Our results indicate that the inhibition of early-stage adipocyte differentiation by sulforaphane may be associated with cell cycle arrest at the G(0)/G(1) phase through upregulation of p27 expression.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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