中文摘要：

为了探讨Notch1信号通路在ERα诱导NCI-H23增殖中的作用,将NCI-H23非小细胞肺癌细胞经E2、DATP或siRNA干预后,采用MTT、细胞集落分析、PI分析、western blotting的方法检测细胞的增殖和蛋白表达变化.结果与空白对照相比E2使细胞增殖能力加强,处于增殖期细胞比例是对照组的1.33倍,Bcl-2和PCNA表达增加,Bax表达减少;DATP合并E2处理后细胞增殖能力明显下降,与E2作用组相比P〈0.01,增殖期细胞比例是E2组的0.66倍,Bax表达明显增加,细胞生存能力下降;当siRNA沉默Notch1表达后E2再刺激使细胞ERα表达明显低于转染control siRNA组,E2在Notch信号减弱后对细胞增殖的刺激作用被削弱.得出了E2刺激细胞增殖需要Notch信号参与,减少Notch信号传导可以抑制E2对细胞的促增殖作用的结论.

英文摘要：

In order to explore the role of Notch1 signaling pathway in ERα-induced proliferation of NCIH23,this research treats non-small cell lung cancer cells with E2,DATP or siRNA and analyzes the proliferation and protein expression of NCI-H23 by MTT,colony assay,PI assay and western blotting. The results show that E2 can enhance the proliferative ability with the proportion of NCI-H23 at S phase 1. 33 fold of the controlled group. The expressions of Bcl-2 and PCNA in E2-treated cells are higher than the non-treated and Bax expression is decreased. The proliferative ability of DATP combined with E2 treatment declines evidently with P 〈 0. 01 and the cell proliferative proportion 0. 66 time of E2 group. With the obvious increase of BAX expression and the decrease of cell viability,before treatment with E2 transfection Notch1 siRNA in NCI-H23,the results show that ERα expression is lower than the controlled siRNA. Thus it draws the conclusion that Notch signaling affects the E2-stimulated cell proliferation and the inhibition of Notch signaling can impair the influence of E2 in NCI-H23.