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首页> 美国卫生研究院文献>International Journal of Clinical and Experimental Pathology >c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer
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c-Myc-activated long non-coding RNA H19 downregulates miR-107 and promotes cell cycle progression of non-small cell lung cancer

机译：c-Myc激活的长非编码RNA H19下调miR-107并促进非小细胞肺癌的细胞周期进程

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To verify c-Myc can regulate the expression of lncRNA H19 directly in non-small cell lung cancer (NSCLC) and clarify the molecular mechanism on how lncRNA H19 promote the cell cycle progression of NSCLC. The mRNA levels of lncRNA H19 in NSCLC tissues and cells, the adjacent tissues and normal cells were determined by RT-PCR. The expression change of lncRNA H19 in NSCLC cells after transfection with pcDNA3.1-c-Myc or c-Myc-siRNA was determined by RT-PCR, respectively. Targeted role of c-Myc on the promoter of H19 was studied by luciferase reporter assay. Chromosome immune coprecipitation (ChIP) was used to confirm the relationship between c-Myc and H19. MiRNAs that have base-pairing with H19 was predicted by online software. The relationship between H19 and miR-107 was determined by disturbing and overexpressing the expression of H19. The influence of the changes of H19 and miR-107 on cell cycle progression was determined by flow cytometry. The mRNA levels of lncRNA H19 in NSCLC tissues and cells were significantly higher than the adjacent tissues and normal cells, respectively. The expression of H19 increased or decreased accordingly with the overexpression and knockdown of c-Myc. The activity of the promoter of H19 was strengthened by c-Myc. While the expression of miR-107 increased or decreased with the overexpression and knockdown of H19, respectively. The number of cells in G2/M stage decreased significantly with the knockdown of H19 and miR-107 compared with the control group. Our study demonstrates that lncRNA H19, which is induced by c-Myc, is up-regulated in NSCLC. H19 influences the mitotic progression of NSCLC cell lines.
机译：为了验证c-Myc可以直接调节非小细胞肺癌（NSCLC）中lncRNA H19的表达，并阐明lncRNA H19如何促进NSCLC细胞周期进程的分子机制。用RT-PCR检测NSCLC组织和细胞，邻近组织和正常细胞中lncRNA H19的mRNA水平。通过RT-PCR分别检测了转染pcDNA3.1-c-Myc或c-Myc-siRNA后NSCLC细胞中lncRNA H19的表达变化。通过萤光素酶报告基因分析研究了c-Myc对H19启动子的靶向作用。使用染色体免疫共沉淀（ChIP）来确认c-Myc与H19之间的关系。在线软件预测了与H19碱基配对的MiRNA。通过干扰和过表达H19的表达来确定H19和miR-107之间的关系。通过流式细胞术确定H19和miR-107的变化对细胞周期进程的影响。 NSCLC组织和细胞中lncRNA H19的mRNA水平分别显着高于邻近组织和正常细胞。 H19的表达随c-Myc的过表达和敲低而相应增加或减少。 H19启动子的活性被c-Myc增强。而miR-107的表达分别随H19的过表达和敲低而增加或减少。与对照组相比，随着H19和miR-107的敲低，G2 / M期的细胞数量明显减少。我们的研究表明，c-Myc诱导的lncRNA H19在NSCLC中被上调。 H19影响NSCLC细胞系的有丝分裂进程。

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