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目的研究绿茶提取物表没食子儿茶素-3-没食子酸酯(Epigallocatechin-3 gallste,EGCG)对人卵巢癌HO-8910细胞增殖及细胞内Wnt/β-catenin信号通路相关基因表达的影响,探讨EGCG抑制卵巢癌细胞生长的机制。方法用不同浓度的EGCG(10、20和40μg/ml)处理体外培养的人卵巢癌HO-8910细胞不同时间(24、48和72 h),采用MTT法检测细胞的增殖活力;流式细胞术检测细胞周期的变化;RT-PCR和Western blot分别检测细胞中β-catenin和下游靶基因CyclinD1 mRNA的转录水平和蛋白的表达水平。结果 EGCG可明显抑制HO-8910细胞的增殖活力,且抑制作用呈剂量-时间依赖性(P<0.05);40μg/ml EGCG干预后,HO-8910细胞主要阻滞于G0/G1期,且在48 h阻滞作用最为明显;EGCG可显著降低HO-8910细胞中β-catenin和CyclinD1基因mRNA的转录水平和蛋白的表达水平,且呈剂量-时间依赖性(P<0.01)。结论 EGCG可抑制HO-8910细胞的增殖,其机制可能与其抑制Wnt/β-catenin信号通路的活性有关,提示EGCG可能在卵巢癌的治疗中具有一定的应用前景。
Objective To investigate the effects of epigallocatechin-3 gallste (EGCG), a green tea extract, on the proliferation of human ovarian cancer HO-8910 cells and the expression of Wnt / β-catenin signaling pathway related genes Mechanisms of EGCG inhibiting the growth of ovarian cancer cells. Methods Human ovarian cancer HO-8910 cells were treated with different concentrations of EGCG (10, 20 and 40 μg / ml) for different time periods (24, 48 and 72 h), respectively. MTT assay was used to detect cell viability. Flow cytometry The changes of cell cycle were detected by RT-PCR and Western blot respectively. The transcription level and protein expression of β-catenin and the downstream target gene CyclinD1 mRNA were detected by RT-PCR and Western blot respectively. Results EGCG significantly inhibited the proliferation of HO-8910 cells in a time-and dose-dependent manner (P <0.05). After 40μg / ml EGCG treatment, HO-8910 cells mainly arrested in G0 / G1 phase, 48 h after transfection. EGCG significantly reduced the mRNA and protein expression of β-catenin and CyclinD1 in HO-8910 cells in a dose-time-dependent manner (P <0.01). Conclusion EGCG can inhibit the proliferation of HO-8910 cells, and its mechanism may be related to the inhibition of the activity of Wnt / β-catenin signaling pathway, suggesting that EGCG may have some application prospects in the treatment of ovarian cancer.