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Effects of diosgenin on cell proliferation induced by IGF-1 in primary human thyrocytes
Dezhi Bian1, Zhiwei Li, Hongyan Ma
1Provincial Hospital Affiliated to Shandong University, Jinan 250021, China.
Abstract:
Others and our previous studies showed that the increase of IGF-1 was involved in the formation of goiter. Our aim here was to evaluate the possible effects of diosgenin on cell proliferation induced by IGF-1 in primary human thyroid cells. The cells were treated with or without different concentrations of diosgenin in the present or absent of IGF-1 for 24, 48 and 72 h, respectively. Cell viability was determined by MTT, and cell proliferation was tested by EdU assay, and cell cycle analysis was performed by FACS. In addition, Cyclin D1 and B1 protein expression was tested by Western Blotting, respectively. We found that IGF-1 promoted cell cycle progression to S phase and increased the primary human thyroid cells proliferation. Diosgenin decreased the protein expression of cyclin D1 and resulted in cell G(0)/G(1) arrest. Importantly, when the human thyrocytes were exposed to diosgenin in the present of IGF-1, the IGF-1 inducing proliferation was significantly decreased and the proportion of the cells in G(0)/G(1) phase was increased, while that of S phase was decreased. This study shows that diosgenin inhibited cell proliferation, caused G(0)/G(1) arrest, and could inhibit cell proliferation induced by IGF-1 in primary human thyroid cells.
Insights
Diosgenin inhibits human thyroid cell proliferation and blocks cell cycle progression. It also counteracts the growth-promoting effects of Insulin-like Growth Factor 1 (IGF-1), suggesting a therapeutic role in thyroid disorders.
Area of Science:
- Endocrinology
- Molecular Biology
- Cell Biology
Background:
- Insulin-like Growth Factor 1 (IGF-1) is implicated in goiter formation.
- Understanding factors that modulate thyroid cell proliferation is crucial for thyroid disease research.
Purpose of the Study:
- To investigate the effects of diosgenin on IGF-1-induced proliferation in primary human thyroid cells.
- To elucidate the molecular mechanisms underlying diosgenin's action on thyroid cell cycle.
Main Methods:
- Primary human thyrocytes were treated with diosgenin and/or IGF-1.
- Cell viability assessed using MTT assay.
- Cell proliferation evaluated by EdU assay.
- Cell cycle distribution analyzed via FACS.
- Protein expression of Cyclin D1 and B1 determined by Western Blotting.
Main Results:
- IGF-1 significantly promoted thyroid cell proliferation and cell cycle progression into S phase.
- Diosgenin treatment led to decreased Cyclin D1 expression and induced G(0)/G(1) cell cycle arrest.
- Diosgenin effectively inhibited IGF-1-induced proliferation and reversed the S phase increase in human thyrocytes.
Conclusions:
- Diosgenin exhibits antiproliferative effects on primary human thyroid cells.
- Diosgenin induces G(0)/G(1) cell cycle arrest.
- Diosgenin can inhibit IGF-1-mediated thyroid cell proliferation, offering potential for therapeutic intervention.
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