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作 者:赵智凝[1] 刘楠[1] 赵晓余[1] 周玉宝[1] 何芙蓉[1]
出 处:《现代生物医学进展》2015年第25期4842-4847,共6页Progress in Modern Biomedicine
基 金:国家重点基础研究发展计划(973计划)资助项目(2010CB529905)
摘 要: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 clarify the potential role and the mechanism of mi R-106b-93-25 cluster on the proliferation and apoptosis of endometrial cancer cells(EMC). Methods: Quantitative real-time polymerase chain reaction(q RT-PCR) was employed to verify the differential expression of the mi RNA cluster mi R-106b-93-25(comprised of mi R-106 b, mi R-93 and mi R-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 mi RNA mimics and inhibitors, dual luciferase reporter assays was used to confirm that p21 and Bim are the target genes of mi R-106 b and mi R-93, respectively. Results: The mi R-106b-93-25 cluster and its host gene MCM7 were obviously upregulated in clinical EMC samples. The mi R-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 mi R-106 b and mi R-93 while the over-expression of mi R-25 resulted in the decrease of cell apoptosis. It indicated that mi R106b-93-25 cluster promote cell division and suppress apoptosis by their target gene p21 and Bim, respectively. Conclusions: The mi R-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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