姜黄素对食管癌细胞中上皮间质转化标志基因表达的影响及Notch、Wnt通路的调节作用

目的探讨姜黄素对食管癌细胞中上皮间质转化(EMT)标志基因表达的影响及Notch、Wnt通路的调节作用。方法选择食管癌Eca-109细胞株进行培养并分为空白对照组及不同剂量姜黄素组(20μmol/L、40μmol/L、80μmol/L、160μmol/L),处理24 h后测定细胞中EMT标志基因、Notch通路基因、Wnt通路基因的表达量。结果不同剂量姜黄素组的细胞中E-钙黏蛋白(E-cadherin)、糖原合成酶激酶-3β(GSK-3β)的m RNA表达量明显高于空白对照组(P<0.05),N-钙黏蛋白(N-cadherin)、波形蛋白(Vimentin)、Notch1、Jagged1、发状分裂相关增强子(HES)、Wnt1、β-连环蛋白(β-catenin)的mRNA表达量明显低于空白对照组(P<0.05);其中160μmol/L姜黄素组细胞中E-cadherin、GSK-3β的m RNA表达量分别为2.05±0.42、2.85±0.48明显高于其他各组(P<0.05),N-cadherin、Vimentin、Notch1、Jagged1、Hes、Wnt1、β-catenin的mRNA表达量分别为0.45±0.08、0.39±0.06、0.39±0.05、0.44±0.07、0.52±0.06、0.41±0.07、0.29±0.05明显低于其他各组(P<0.05)。结论姜黄素能够通过抑制Notch通路、Wnt通路来阻碍食管癌细胞中的EMT过程。

Regulatory Effect of Epithelial-Mesenchymal Transition Marker Genes in Esophageal Cancer Cells Influence of Expression and Regulation of Notch and Wnt Pathways

Objective To study the regulatory effect of curcumin on the expression of epithelial-mesenchymal transition marker genes and Notch,Wnt pathways in esophageal carcinoma cells.Methods Esophageal carcinoma Eca-109 cell line was cultured and divided into a blank control group and a curcumin group(20μmol/L,40μmol/L,80μmol/L,160μmol/L).The expression of epithelial-mesenchymal transition marker gene,Notch pathway gene and Wnt pathway gene was measured 24 hours after treatment.Results The mRNA expression of E-cadherin and GSK-3βin curcumin group were significantly higher than those of blank control group(P<0.05),and the mRNA expression of N-cadherin,Vimentin,Notch1,Jagged1,HES,Wnt1 andβ-catenin were significantly lower than those of blank control group(P<0.05).The mRNA expression of E-cadherin,GSK-3βin 160μmol/L curcumin group were(2.05±0.42),(2.85±0.48)respectively and significantly higher than other groups;the m RNA expression of N-cadherin,Vimentin,Notch1,Jagged1,Hes,Wnt1 andβ-catenin were(0.45±0.08),(0.39±0.06),(0.39±0.05),(0.44±0.07),(0.41±0.07),(0.29±0.05)respectively and were significantly lower than other groups(P<0.05).Conclusion Curcumin can inhibit the epithelial-mesenchymal transformation of esophageal cancer cells by inhibiting Notch and Wnt pathways.