摘要
目的探讨miR-183及Akt1蛋白在子宫内膜癌(EC)组织中的表达,以及抑制或过表达miR-183对Ishikawa细胞内Akt1蛋白表达的影响。方法实时定量PCR方法检测子宫内膜癌组织miR-183及Akt1m RNA的表达水平,Western blot方法检测子宫内膜癌组织Akt1蛋白表达;将miR-183 inhibitors或miR-183 mimics应用阳离子脂质体Lipofectamine TM2000转染将转染至Ishikawa细胞,实时定量PCR方法及Western blot方法分别检测转染后Akt1 mRNA及蛋白的表达变化,MTT方法检测转染后细胞增殖能力的变化。结果 miR-183在子宫内膜癌组织中的表达量较癌旁组织明显降低,Akt1蛋白及mRNA在癌组织中较癌旁组织表达明显增高(P<0.01);与对照组相比,转染miR-183 mimics的Ishikawa细胞内Akt1蛋白与mRNA水平显著降低,细胞增殖能力显著下降(P<0.01);与对照组相比,转染miR-183 inhibitors的Ishikawa细胞内Akt1蛋白与mRNA水平显著升高,细胞增殖能力亦显著升高(P<0.01)。结论 miR-183在子宫内膜癌组织中低表达,并能够抑制Ishikawa细胞增殖,抑制Akt1的表达可能是其作用机制之一。
Objective To study the expressions of miR-183 and Aktl protein in endometrial carcinoma（EC） tissues and the effect of inhibitors or mimics of miR-183 on the expression of Aktl in Ishikawa cell. Methods The expression of miR-183 and Aktl mRNA in EC tissues was detected by real-time quantitative PCR, the expression of Aktl was detected by Western blot. The expression of Aktl and Aktl mRNA was detected by Western blot and real-time quantitative PCR respectively after the miR-183 inhibitors or miR-183 mimics was transfected into Ishikawa cell, the cell proliferation was analyzed by MTT assay. Results The expression level of miR-183 was significantly decreased in endometrial carcinoma tissues than in normal tissues, and the expression levels of Aktl protein and mRNA were significantly higher in cancer tissues than in normal tissues（P〈0.01）. The expression levels of Aktl protein and mRNA, as well as cell proliferation were increased significantly after miR-183 inhibitors was transfeeted into Ishikawa cells, and but were decreased significantly after miR-183 mimics were transfeeted into Ishikawa cell（P〈0.01）. Conclusion The low expression of miR-183 in EC tissues inhibited Ishikawa cells proliferation the expression of Aktl.
出处
《解剖科学进展》
2017年第1期50-53,共4页
Progress of Anatomical Sciences
基金
国家自然科学青年基金(81602589)
