中文摘要：

目的 观察RORα高表达对MGC803细胞增殖与迁移侵袭的影响。方法 构建高表达RORα人胃癌MGC803细胞。Real-time PCR或RT-PCR和Western blot检测RORα、MMP-9与TIMP3 m RNA和蛋白表达。MTT、流式细胞术、迁移和侵袭实验检测RORα高表达对MGC803细胞增殖、细胞周期、迁移和侵袭能力的影响。结果 RORα高表达MGC803细胞RORαm RNA和蛋白表达显著上调。在48、72与96 h,RORα高表达细胞的增殖活性明显低于对照组和空载体组（P〈0.05）。RORα高表达G_2/M期细胞明显高于对照组和空载体组（P〈0.05）。高表达组细胞的迁移距离较对照组与空载体组明显减少（P〈0.05）。高表达组穿膜细胞数较对照组与空载体组明显减少（P〈0.05）。RORα高表达可明显下调MMP-9和上调TIMP3m RNA与蛋白。结论 成功构建RORα高表达MGC803细胞,RORα高表达可抑制MGC803细胞增殖与迁移侵袭,将细胞阻滞于G2/M期,其机制可能与下调MMP-9和上调TIMP3有关。

英文摘要：

Objective To investigate the effect of RORct overexpression on human gastric cancer MGC803 cells proliferation, migration and invasion. Methods The expressions of RORct, MMP-9 and TIMP3 mRNA and protein were detected by Real-time PCR or RT-PCR and Western blot. The effect of RORct overexpression on the proliferation, cell cycle, migration and invasion of MGC803 cells were detected by MTf, flow cytometry, wound healing and Transwell assays. Results The expressions of RORa mRNA and protein were stably increased in the RORa/MGC803 cells. The proliferation activity in RORa/MGC803 cells were notably lower than in MGC803 cells and in vector/MGC803, respectively, at 48 h,72 h and 96 h（P〈0.05）. Percentage of G2/M in RORa/MGC803 cells markedly higher than that in MGC803 cells and vector/MGC803（P〈0.05）. The migration length in RORtt/MGC~03 cells was markedly lower than that in MGC803 and vector/MGC803 cells （P〈0.05）. The cells through the matrigel coated membrane in RORa/MGC803 significantly decreased comparing with MGC803 and vector/MGC803 cells（P〈0.05）. RORct overexpression was downregulation of MMP-9 and upregulation of TIMP3 mRNA and proteins（P〈0.05）. RORa overexpression could significantly downregulate MMP-9 and upregulate TIMP3 mRNA and proteins（P〈0.05）. Conclusion RORa/MGC803 cells with stably overexpressed RORa are successfully constructed. The overexpression of RORa may inhibit the proliferation, migration and invasion, as well as G2/M arrest in MGC803 cells, which may be correlated with the downregulation of MMP-9 and the upregulation of TIMP3.