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目的：检测miR-106b-93-25 基因簇对子宫内膜癌细胞增殖及凋亡的影响，并探讨其机制。方法：qRT-PCR 检测临床子宫内膜癌标本及癌旁正常组织中miR-106b、miR-93 和miR-25 及其宿主基因MCM7 的表达情况。将microRNA 及其拮抗剂转染ECC-1 细胞后，MTT 实验检测ECC-1 细胞增殖情况，流式细胞术检测ECC-1 细胞周期及细胞凋亡情况。荧光素酶报告系统验证 miR-106b 和miR-25 分别直接调控p21 和Bim。结果：临床标本子宫内膜癌组织与癌旁正常组织相比miR-106b-93-25 簇及其宿主基因MCM7 的表达明显增高。miR-106b-93-25 簇能够促进ECC-1 细胞增殖，减少凋亡。转染miR-106b和miR-93 的细胞出现明显的S期阻滞，过表达miR-25的细胞凋亡明显减少。miR-106b-93-25 簇通过抑制靶基因p21 和Bim 的表达，引起促增殖、抗凋亡作用。结论：miR-106b-93-25簇能够促进子宫内膜癌细胞增殖，抑制凋亡，并使细胞发生S期阻滞。miR-106b-93-25 簇在子宫内膜癌的发生与发展中具有重要的作用。

英文摘要:

Objective:To clarify the potential role and the mechanism of miR-106b-93-25 cluster on the proliferation and apoptosis of endometrial cancer cells (EMC).Methods:Quantitative real-time polymerase chain reaction (qRT-PCR) was employed to verify the differential expression of the miRNA cluster miR-106b-93-25 (comprised of miR-106b, miR-93 and miR-25) and its host gene MCM7 in clinical EMC samples and adjacent normal tissues. Cell cycle, apoptosis and cell growth of EMC cells were determined by FACS and MTT assays after transfected of miRNA mimics and inhibitors, dual luciferase reporter assays was used to confirm that p21 and Bim are the target genes of miR-106b and miR-93, respectively.Results:The miR-106b-93-25 cluster and its host gene MCM7 were obviously upregulated in clinical EMC samples. The miR-106b-93-25 cluster promotes the proliferation and attenuates the apoptosis of ECC-1 cells. The cell-cycle progression was blocked at S phase after treated with miR-106b and miR-93 while the over-expression of miR-25 resulted in the decrease of cell apoptosis. It indicated that miR106b-93-25 cluster promote cell division and suppress apoptosis by their target gene p21 and Bim, respectively.Conclusion:The miR-106b-93-25 cluster promotes EMC cell growth and inhibited cell apoptosis and cell cycle arrest. This cluster plays an important role on the generation and progression of EMC.

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