期刊
JOURNAL OF RECEPTORS AND SIGNAL TRANSDUCTION
卷 29, 期 6, 页码 293-298出版社
TAYLOR & FRANCIS LTD
DOI: 10.3109/10799890903241824
关键词
Pancreatic beta-cell proliferation; FoxO; glucose; Bcl-6; cyclin D2
资金
- Swiss National Foundation [3100A0-102147/1]
- Fondation pour Recherches Medicales, Geneva
Lack of nutrients and growth factors activates FoxO transcription factors in pancreatic beta-cells, whereas P13K/Akt-dependent inactivation of FoxO favors proliferation. To address the link between FoxO and cell cycle control, we deprived Min6 cells of serum and glucose which activated FoxO and inhibited proliferation. Concomitantly, expression of the transcriptional repressor Bcl-6 was stimulated, whereas cyclin D2 was lowered. Gain of function approaches indicated that FoxO activation was sufficient to activate bcl-6 transcription, while Bcl-6 repressed cyclin D2 transcription and proliferation. Thus, in pancreatic beta-cells, the FoxO/Bcl6/cyclin D2 pathway connects nutrient and growth factor status to cell cycle control, and may therefore be considered for its therapeutic potential in diabetes.
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