微小RNA-125b、27a对肺癌细胞95D靶基因的调控

Target Gene Regulation of MicroRNA-125b and MicroRNA-27a in Lung Cancer 95D Cells

  • 摘要:
    目的 探讨微小RNA(miR)-125b和miR-27a对肺癌细胞95D靶基因的调控作用,探索肺癌的发病机制。
    方法 通过生物信息学对miR-125b和miR-27a进行靶基因预测和GO功能分析,并通过转染模拟物和抑制物的分别上调和下调细胞中miR-125b和miR-27a的表达水平,应用Western blot检测预测靶基因的蛋白表达水平。
    结果 靶基因预测和GO基因功能注释结果显示:miR-125b与凋亡的调节功能有关,MAP3K11是其重要靶基因之一;miR-27a与转录和细胞分化功能有关,PLK2是其潜在靶基因之一。Western blot结果显示:与相应阴性对照组相比,miR-125b抑制物转染组MAP3K11蛋白的表达明显增高1.795倍(P < 0.05),模拟物转染组MAP3K11蛋白的表达未发生明显改变(P>0.05);miR-27a抑制物和模拟物转染组PLK2蛋白的表达均未发生明显改变(P>0.05)。
    结论 miR-125b可能通过对MAP3K11的调节参与MAP3K介导的凋亡,影响肺癌的发生发展。

     

    Abstract:
    Objective To examine the regulation of microRNA (miR)-125b and miR-27a to target genes in lung cancer 95D cells and related mechanism.
    Methods The target genes and GO function of miR-125b and miR-27a were predicted and analyzed by bioinformatics analysis. The expression levels of miR-125b and miR-27a were up-regulated and down-regulated by transfecting mimics and inhibitors in cells, respectively. Then the protein expression levels of predicted target genes were detected using Western blot.
    Results According to the results of target genes prediction and GO function analysis, miR-125b was associated with the apoptosis regulation of MAP3K, and MAP3K11 was one of the important target genes. In addition, miR-27a was associated with transcription and cell differentiation function, and PLK2 was one of the potential target genes. The results of Western blot showed that, compared with the negative control group, the protein expression of MAP3K11 of the miR-125b inhibitors transfection group significantly increased by 1.795 times (P < 0.05), but that of the miR-125b mimics transfection group did not obviously change (P>0.05). Moreover, the protein expression of PLK2 of the miR-27a inhibitors and the mimics transfection groups did not significantly change (P>0.05).
    Conclusion The study findings indicate that miR-125b may participate in MAP3K mediated apoptosis and affect lung cancer development via regulating MAP3K11.

     

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