Objective To investigate the growth activities and the background changes of PBK/Akt/mTOR pathway with the stimulation of IGF-1 in Rhl sarcoma cells. Methods Rhl cells were cultured with 10% FBS RPMI1640 media to firstly abolish the effect of the inner substances, the cells were starved with the pure RPMI1640 for 27 h, then the IGF-1 was added (final concentration 10 ng/ml) for stimulating 5, 10, 20, 30 and 60 minutes separately. The flow cytometer was used to determine the cell growth activities and western blot method was used to observe dynamic changes of Akt (s473) and S6. Results Compared to control, IGF-1 could promote the survival of Rhl cells. The phosphorylation of S6 was increased gradually. IGF-1 also could give rise to the phosphorylation of Akt (s473). And the peak of phosphorylation was present at 5 minutes, and then decreased gradually. Conclusions With the stimulation of IGF-1, the increased dynamic changes of S6 and the decreased dynamic changes of Akt (s473) exist in Rhl cells.%目的 探讨胰岛素样生长因子(IGF)1对Rh1肉瘤细胞生长活性和PI3 K/Akt/mTOR信号通路的背景变化.方法 常规细胞培养,用无血清培养基消除内源性因子影响27h,再用IGF-1(终浓度为10 ng/ml)刺激72 h,流式细胞仪检测细胞生长活性；另外Western印迹方法观察IGF-1刺激细胞5、10、20、30和60min后Akt(s473)、S6的动态变化.结果 与对照组相比,IGF-1可促进Rh1细胞存活.IGF-1刺激不同时间后S6磷酸化则随着时间的延长逐渐增强；IGF-1亦导致Akt(s473)位点的磷酸化,随时间的延长,磷酸化Akt在5min时达高峰,此后逐渐减弱.结论 Akt、S6等是PI3K/Akt/mTOR信号通路中的重要信号分子,对Rhl细胞而言,在IGF-1刺激下S6有逐渐增强的变化,Akt (s473)位点磷酸化则有减弱的动态变化.
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