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目的:检测mi R-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:q RT-PCR检测临床子宫内膜癌标本及癌旁正常组织中mi R-106b、mi R-93和mi R-25及其宿主基因MCM7的表达情况。将micro RNA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mi R-106b和mi R-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mi R-106b-93-25簇及其宿主基因MCM7的表达明显增高。mi R-106b-93-25簇能够促进ECC-1细胞增殖,减少凋亡。转染mi R-106b和mi R-93的细胞出现明显的S期阻滞,过表达mi R-25的细胞凋亡明显减少。mi R-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:mi R-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。mi R-106b-93-25簇在子宫内膜癌的发生与发展中具有重要的作用。
Objective: To investigate the effect of mi R-106b-93-25 gene cluster on the proliferation and apoptosis of endometrial carcinoma cells and to explore its mechanism. Methods: The expression of mi R-106b, mi R-93 and mi R-25 and their host gene MCM7 in clinical endometrial carcinoma and adjacent normal tissues were detected by q RT-PCR. After transfection of microRNA and its antagonist into ECC-1 cells, the proliferation of ECC-1 cells was detected by MTT assay and the cell cycle and apoptosis of ECC-1 cells were detected by flow cytometry. Luciferase reporter system validates that mi R-106b and mi R-25 directly regulate p21 and Bim, respectively. Results: The expression of mi R-106b-93-25 cluster and its host gene MCM7 in clinical specimens of endometrial carcinoma were significantly higher than those in adjacent normal tissues. mi R-106b-93-25 cluster promotes ECC-1 cell proliferation and reduces apoptosis. Significant S phase arrest occurred in cells transfected with mi R-106b and mi R-93, with a marked decrease in mi R-25 overexpression. mi R-106b-93-25 cluster induced proliferation and anti-apoptotic effects by inhibiting the expression of target genes p21 and Bim. Conclusion: The mi R-106b-93-25 cluster can promote the proliferation of endometrial cancer cells, inhibit the apoptosis and arrest the cells in S phase. mi R-106b-93-25 cluster plays an important role in the occurrence and development of endometrial cancer.