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目的观察Sulindac对人肝癌细胞HepG2增殖、凋亡及β-catenin蛋白表达的影响,探讨Sulindac抗肝癌的可能机制。方法不同浓度的Sulindac作用HepG2细胞后,采用MTT实验检测细胞增殖抑制作用;采用Hoechst33258染色法检测Sulindac对HepG2细胞凋亡的影响;利用RT-PCR及Western blotting检测HepG2细胞在Sulindac作用后Wint通路中β-catenin的表达变化。结果 Sulindac对人肝癌细胞HepG2有增殖抑制作用,且呈剂量时间依赖关系;Hoechst33258结果显示,Sulindac作用24 h后HepG2细胞凋亡数目明显增多;随着Sulindac浓度的增加,β-catenin mRNA及蛋白表达量逐渐下降。结论 Sulindac能够抑制人肝癌细胞HepG2增殖,通过阻断Wnt信号传导通路,降低β-catenin表达,诱导人肝癌细胞HepG2的凋亡。
Objective To observe the effects of Sulindac on proliferation, apoptosis and β-catenin protein expression in HepG2 human hepatocellular carcinoma cells and to explore the possible mechanism of Sulindac against hepatocellular carcinoma. Methods Sulindac cells were treated with different concentrations of Sulindac. MTT assay was used to detect the effect of Sulindac on the proliferation of HepG2 cells. The effect of Sulindac on the apoptosis of HepG2 cells was detected by Hoechst33258 staining. The expression of Sulindac in HepG2 cells was detected by RT-PCR and Western blotting. β-catenin expression changes. Results Sulindac inhibited the proliferation of HepG2 cells in a time-and dose-dependent manner. Hoechst33258 showed that the number of apoptotic HepG2 cells increased significantly after Sulindac treatment for 24 h. The mRNA and protein expression of β-catenin increased with the increase of Sulindac concentration The amount gradually decreased. Conclusion Sulindac can inhibit the proliferation of human hepatocellular carcinoma HepG2 cells by blocking the Wnt signaling pathway, decreasing the expression of β-catenin and inducing the apoptosis of HepG2 cells.