[干细胞因子/原癌基因c-Kit信号通路通过磷脂酰肌醇-3激酶途径促进T24细胞侵袭]
[SCF/c-Kit signaling promotes invasion of T24 cells via PI3K pathway].
作者信息
Guo Shujun, Tao Xiangnan, Wang Yimeng, Tang Jie, Shen Lin, Song Chuanwang
机构信息
Department of Immunology/Anhui Provincial Key Laboratory of Infection and Immunity, Bengbu Medical College, Bengbu 233030, China.E-mail:
出版信息
Nan Fang Yi Ke Da Xue Xue Bao. 2014 Apr;34(4):507-10.
OBJECTIVE
To explore the role of SCF/c-Kit signaling in the invasion of bladder cancer T24 cells.
METHODS
Western blotting was used to detect the expression of c-Kit and PI3K pathway activation stimulated by stem cell factor (SCF) in T24 cells. The invasiveness of T24 cells before and after SCF stimulation and Wortmannin (aspecific PI3K inhibitor) treatment was evaluated using Transwell invasion assay (direct and indirect counting methods).
RESULTS
T24 cells expressed c-Kit protein and showed obvious Akt phosphorylation after stimulation with SCF (1 ng/ml) for 24 h. Compared to the control group, SCF stimulation (1 ng/ml) caused a greater number of T24 cells to migrate through the polycarbonate film (P<0.01), and this effect was blocked by the application of Wortmannin before the stimulation.
CONCLUSION
SCF/c-Kit signaling promotes the invasiveness of T24 cells, and this effect is mediated by the PI3K pathway.
目的
探讨干细胞因子（SCF）/c-Kit信号通路在膀胱癌T24细胞侵袭中的作用。
方法
采用蛋白质免疫印迹法检测T24细胞中c-Kit的表达以及干细胞因子（SCF）刺激后PI3K信号通路的激活情况。使用Transwell侵袭实验（直接计数法和间接计数法）评估SCF刺激及渥曼青霉素（一种特异性PI3K抑制剂）处理前后T24细胞的侵袭能力。
结果
T24细胞表达c-Kit蛋白，在1 ng/ml SCF刺激24小时后，Akt磷酸化明显。与对照组相比，1 ng/ml SCF刺激使更多T24细胞穿过聚碳酸酯膜（P<0.01），且在刺激前应用渥曼青霉素可阻断此效应。
结论
SCF/c-Kit信号通路促进T24细胞的侵袭能力，且此效应由PI3K信号通路介导。
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