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目的探讨Jagged1调控STAT 3对卵巢癌A 2780细胞迁移能力的影响。方法 Notch信号特异性阻断剂γ-分泌酶抑制剂(N-[N-(3,5-difluorophenacetyl)-1-alanyl]-S-phenylglycine t-butyl ester,DAPT)以浓度梯度的方式(0μM、2.5μM、5μM、10μM、20μM和40μM)处理卵巢癌A 2780细胞,通过CCK-8和平板克隆实验分析细胞增殖能力,Transwell迁移实验和体外划痕实验检测A 2780细胞迁移能力,Western blot检测Jagged1、STAT 3和p-STAT 3的蛋白表达。结果实验组细胞的平板克隆形成能力均低于对照组细胞,且随浓度升高呈逐级递减趋势,且10μM DAPT处理后的细胞下降最明显(P<0.05)。实验组的迁移能力明显低于对照组,且呈时间梯度和浓度梯度的方式降低(P<0.05)。卵巢癌A 2780细胞中Jagged1下调p-STAT 3表达以浓度和时间依赖的方式,DAPT浓度大于10μM有明显抑制作用(P<0.05);STAT 3蛋白表达的作用变化无明显差异(P>0.05)。结论抑制Jagged1可下调STAT 3导致卵巢癌A 2780细胞活力、增殖和迁移能力降低,Jagged1可能成为卵巢癌治疗的潜在新靶点。
Objective To investigate the effect of Jagged1 regulating STAT3 on the migration of ovarian cancer A 2780 cells. Methods Notch signal-specific blocker γ-secretase inhibitor (N- [N- (3,5-difluorophenacetyl) -1-alanyl] -S-phenylglycine t-butyl ester (DAPT) The proliferation of A 2780 cells was detected by CCK-8 and plate cloning experiments. The migration ability of A 2780 cells was detected by Transwell migration assay and in vitro scratch assay. The migration of A 2780 cells was detected by Western blot Jagged1, STAT3 and p-STAT3 protein expression. Results The clonal formation ability of the cells in the experimental group was lower than that in the control group, and decreased progressively with the increase of the concentration, and the most significant decrease was observed in the cells treated with 10μM DAPT (P <0.05). Migration of the experimental group was significantly lower than the control group, and the time gradient and concentration gradient manner (P <0.05). Overexpression of Jagged1 reduced the expression of p-STAT3 in ovarian cancer A 2780 cells in a concentration-dependent and time-dependent manner (P <0.05). The effect of STAT3 protein expression was not significantly different (P> 0.05) . Conclusions Inhibition of Jagged1 can down-regulate STAT3, resulting in decreased viability, proliferation and migration of ovarian cancer A 2780 cells. Jagged1 may be a potential new target for the treatment of ovarian cancer.