目的:探讨子宫内膜癌RL-95-2细胞中let-7g对其靶基因视网膜母细胞瘤相关蛋白1(retinoblastoma-associated protein 1,RB1)表达的调控作用。方法:运用生物信息学方法对let-7g进行靶基因预测并分析其靶基因RB1;let-7g模拟物(let-7g mimic)、模拟物对照组(mimic control)、let-7g抑制物(let-7g inhibitor)、抑制物对照组(inhibitor control)分别转染至RL-95-2细胞,采用CCK-8法检测其对细胞增殖的影响;实时荧光定量PCR(real-time quantitative polymerase chain reaction,RT-qPCR)检测转染后RB1 mRNA的表达差异;Western blotting检测RB1蛋白的表达。结果:RB13’非编码区(3’UTR)含有一个let-7g结合位点,而且该结合位点在多个物种中高度保守;与未转染组相比,转染let-7g mimic可促进细胞增殖,且使RB1蛋白的表达显著降低,而转染let-7g抑制物则抑制细胞增殖,使RB1蛋白的表达显著增高,其余各组无明显变化;而各转染组RB1 mRNA表达无明显差异。结论:子宫内膜癌RL-95-2细胞中let-7g可以结合到RB1的3’UTR,负性调控RB1的表达,从而促进细胞生长。 Objective: To investigate the regulatory effect of let-7g on the expression of its target gene retinoblastoma-associated protein 1 (RB1) in endometrial carcinoma RL-95-2 cells. Methods: The gene targeting let-7g was predicted by bioinformatics method and the expression of let-7g let-7g mimic, mimic control, let-7g inhibitor -7g inhibitor and inhibitor control were transfected into RL-95-2 cells respectively. The effect of CCK-8 on cell proliferation was detected by real-time quantitative polymerase chain reaction (RT-PCR) RT-qPCR) were used to detect the expression of RB1 mRNA. The expression of RB1 protein was detected by Western blotting. Results: The RB13 ’non-coding region (3’UTR) contained a let-7g binding site and the binding site was highly conserved among multiple species. Transfection with let-7g mimic compared with untransfected group promoted While the expression of RB1 protein was significantly decreased. However, the let-7g inhibitor transfected cells inhibited the cell proliferation, and the expression of RB1 protein was significantly increased, while the other groups had no significant change; while the expression of RB1 mRNA in each transfected group was not significant difference. Conclusion: let-7g can bind to 3’UTR of RB1 in endometrial carcinoma RL-95-2 cells and negatively regulate RB1 expression to promote cell growth.