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目的:研究孤儿核受体ERRα对前列腺癌细胞E-cadherin(上皮细胞钙粘蛋白)的表达水平和体内转移能力的影响。方法:利用慢病毒介导的sh RNA构建稳定下调ERRα表达的DU145-sh ERRα和PC-3M-sh ERRα前列腺癌细胞模型,同时用ERRα特异性抑制剂XCT790抑制其活性,并利用Western Blotting(免疫印迹)检测上皮细胞标志物E-cadherin的表达水平。将PC-3M-sh ERRα细胞和PC-3M-scramble对照细胞用荧光素酶标记后原位注射小鼠前列腺,8周以后通过体内成像系统检测原位瘤的形成及其体内转移情况。结果:基因沉默ERRα表达水平和用其特异性抑制剂XCT790处理DU145后,E-cadherin的表达水平明显降低。在PC-3M-sh ERRα细胞中,E-cadherin的表达水平明显低于对照组,同时由其构建的6只原位前列腺癌小鼠模型中没有发生转移,而由对照组细胞构建的7只原位前列腺癌小鼠模型中有4只发生了转移。结论:在前列腺癌细胞中下调ERRα的表达水平抑制其E-cadherin的表达和体内转移能力。
Objective: To investigate the effect of orphan nuclear receptor ERRα on the expression of E-cadherin (E-cadherin) and the ability of metastasis in vivo. METHODS: DU145-sh ERRα and PC-3M-sh ERRα prostate cancer cell lines stably down-regulated ERRα expression were constructed by lentivirus-mediated sh RNA. Meanwhile, ERRα-specific inhibitor XCT790 was used to inhibit its activity. Western Blotting Blotting) to detect the expression of epithelial marker E-cadherin. PC-3M-sh ERRα cells and PC-3M-scramble control cells were labeled with luciferase and injected into the prostate of mice in situ. After 8 weeks, the in situ tumor formation and metastasis in vivo were detected by in vivo imaging system. Results: E-cadherin expression was significantly decreased after ERRα gene silencing and DU145 treatment with its specific inhibitor XCT790. The expression level of E-cadherin in PC-3M-sh ERRα cells was significantly lower than that in the control group, and no metastasis was found in the 6 in situ prostate cancer mouse models constructed by it, while 7 Four of the in situ prostate cancer mouse models had metastases. Conclusion: Down-regulation of ERRα expression in prostate cancer cells inhibits the expression of E-cadherin and the ability of metastasis in vivo.