miR-122通过介导sprouty2调控肾癌细胞的增殖

发布时间：2018-05-26 09:56

本文选题：miR- + sprouty　；参考：《南京医科大学学报(自然科学版)》2015年04期

【摘要】：目的 :研究mi R-122在肾癌发生中的作用以及与sprouty2之间的关系。方法 :通过RT-q PCR实验,测定32对肾癌组织及邻近癌旁组织中mi R-122的表达水平。将mi R-122抑制剂(mi R-122 inhibitor)转染至肾癌细胞株786-0和CAKI-1中,下调mi R-122的表达,在不同时间点,CCK-8实验检测细胞增殖,流式细胞仪检测细胞周期,RT-q PCR和Western blot检测sprouty2m RNA和蛋白表达情况。通过双荧光报告素酶基因实验,研究mi R-122与sprouty2 3′UTR结合情况。结果 :mi R-122在肾癌组织中表达明显升高(P0.05);mi R-122 inhibitor转染后能够抑制肾癌细胞增殖(P0.05)及导致细胞周期阻滞(P0.05),并促进肿瘤细胞中sprouty2蛋白的表达(P0.05);双荧光报告素酶基因实验表明mi R-122 inhibitor能与sprouty2 3′UTR结合,显著升高荧光值(P0.05)。结论:mi R-122促进肾癌细胞的增殖,sprouty2可能是mi R-122的靶基因。
[Abstract]:Objective: to study the role of mi R 122 in renal cell carcinoma and its relationship with sprouty2. Methods: the expression of miR-122 in 32 pairs of renal carcinoma tissues and adjacent tissues was determined by RT-q PCR assay. The expression of miR-122 was down-regulated in 786-0 and CAKI-1 cell lines. The cell proliferation was detected by CCK-8 assay at different time points. The expression of sprouty2m RNA and protein in cell cycle RT-q PCR and Western blot were detected by flow cytometry. The binding of miR-122 to sprouty2 3'UTR was studied by double fluorescein reporter gene experiment. Results the cell cycle arrest and the expression of sprouty2 protein were significantly increased in renal cell carcinoma tissues induced by cell cycle arrest (P0.05) and cell cycle arrest (P0.05). Double fluorescein reporter gene assay It shows that mi R-122 inhibitor binds to sprouty2 3'UTR, The fluorescence value was increased significantly (P 0.05). ConclusionThe proliferation of renal cancer cells promoted by: mi-mi R-122 may be the target gene of miR-122.
【作者单位】：南京医科大学第一附属医院泌尿外科;
【基金】：国家自然科学基金面上项目(81372757;81171963) 江苏省科技厅基础研究计划(自然科学基金)(BK2008473)
【分类号】：R737.11

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