表没食子儿茶素没食子酸酯调控CDC25A表达与抑制食管癌细胞增殖作用及机制

Regulating CDC25A Expressing EGCG for Inhibiting Proliferative Action of Esophageal Cancer Cells and Its Mechanism

目的探讨表没食子儿茶素没食子酸酯(epigallocatechin-3-gallate,EGCG)抑制食管癌细胞Ec9706增殖作用及其相关机制。方法流式细胞术检测38例原发性食管鳞癌患者和20例患者正常食管黏膜组织的细胞周期及CDC25A蛋白表达水平。不同质量浓度EGCG(0,100,200,300 mg/L)作用Ec9706细胞24,48 h后流式细胞术检测细胞增殖及CDC25A蛋白表达水平。结果食管癌组织增殖指数为(24.92±11.01)%,显著高于正常食管组织的(14.49±3.83)%(P<0.05);食管癌细胞中CDC25A蛋白表达水平显著高于食管正常组织中的表达水平(P<0.05);不同质量浓度EGCG作用Ec9706细胞24 h后,细胞增殖指数及CDC25A蛋白表达水平显著降低(P<0.05)。结论 CDC25A在食管癌组织中高表达,且参与了食管癌组织高增殖状态的形成,EGCG可通过下调CDC25A表达,抑制食管癌细胞增殖。

Objective To explore the effect and mechanism of epigallocatechin-3-gallate （ EGCG ） in inhibiting the proliferation action of esophageal carcinoma cells Ec9706. Methods The expression level of CDC25A protein and cell cycle were detected by the flow cy-tometry in 38 cases of esophageal squamous cell carcinoma and 20 cases of normal esophageal tissue. At 24, 48 h after treating the Ec9706 cells by different concentrations of EGCG （ 0, 100, 200, 300mg/L ） , the expression level of CDC25A and cell cycle were detect-ed by the flow cytometry. Results The proliferation index （ PI ） in the esophageal cancer tissue was （ 24. 92 ± 11. 01 ） %, which was significantly higher than （ 14. 49 ± 3. 83 ）% in the normal esophageal tissue, the difference was statistically significant （ P 〈 0. 05 ） . The expression level of CDC25A protein in the esophageal carcinoma cells was significantly higher than that in the normal esophageal tissue with statistical difference between them （ P 〈 0. 05 ） . After 24 h different concentrations of EGCG acting on Ec9706 cells, PI and CDC25A protein expression level were decreased significantly, the difference was statistically significant （ P 〈 0. 05 ） . Conclusion The high expression of CDC25A in esophageal cancer tissue could participate in the formation of high proliferation status of esophageal can-cer tissue. EGCG could inhibit the proliferation of esophageal carcinoma cells by down-regulating the expression of CDC25A.