首页> 外文期刊>Molecular medicine reports >Reduced expression of miR-205-5p promotes apoptosis and inhibits proliferation and invasion in lung cancer A549 cells by upregulation of ZEB2 and downregulation of erbB3
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Reduced expression of miR-205-5p promotes apoptosis and inhibits proliferation and invasion in lung cancer A549 cells by upregulation of ZEB2 and downregulation of erbB3

机译:MiR-205-5P的表达降低促进细胞凋亡,抑制Zeb2的上调和erbB3下调的肺癌A549细胞增殖和侵袭

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Previous studies have demonstrated that microRNA (miR)-205-5p expression is significantly increased in non-small cell lung cancer tissues and is associated with tumor differentiation grade. The aim of the present study was to explore the effects of miR-205-5p on viability, apoptosis and invasion of lung cancer A549 cells. The hsa-miR-205-5p small interfering RNA (siRNA) inhibitor was transfected into A549 cells and expression of miR-205-5p was detected by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). Cell viability, apoptosis and invasion were assayed by Cell Counting kit-8, Annexin V/propidium iodide double staining and Transwell assay, respectively. Target genes of miR-205-5p were predicted using bioinformatics analysis. Expression of mRNA and protein levels of candidate target genes following miR-205-5p inhibition were detected using RT-qPCR and western blot analysis respectively. The results demonstrated that relative survival rates of A549 cells were significantly inhibited in miR-205-5p siRNA-transfected cells at 24 and 48 h compared with control cells. Apoptosis was markedly increased in the miR-205-5p siRNA cells compared with control cells. The number of invaded cells following miR-205-5p siRNA silencing was significantly decreased compared with control cells. Bioinformatics analysis revealed that erb-B2 receptor kinase 3 (erbB3), zinc finger E-box binding homeobox 2 (ZEB2), clathrin heavy chain (CLTC) and mediator complex subunit 1 (MED1) may be potential target genes of miR-205-5p. Reduced expression of miR-205-5p significantly increased the expression of ZEB2 mRNA and protein, inhibited the expression of erbB3 protein, but had no significant effect on the expression levels of CLTC and MED1. In summary, reduced expression of miR-205-5p promoted apoptosis and inhibited proliferation and invasion in lung cancer A549 cells through upregulation of ZEB2 and downregulation of erbB3. The present results suggested that the increased miR-205-5p expression observed in non-small cell lung cancer tissues may contribute to increased proliferation and invasion of lung cancer cells and thus to cancer progression.
机译:先前的研究已经表明,微RNA(MIR)-205-5p表达在非小细胞肺癌组织显著增加,并且与肿瘤分化程度相关联。本研究的目的是探讨的miR-205-5p的上存活力,凋亡和肺癌A549细胞的侵袭的影响。的HSA-的miR-205-5p的小干扰RNA(siRNA)抑制剂转染A549细胞,并通过逆转录 - 定量聚合酶链式反应(RT-qPCR的)检测的miR-205-5p的表达。细胞活力,凋亡和侵袭通过细胞计数试剂盒-8,膜联蛋白V /碘化丙啶双染色和Transwell小室法分别测定。的miR-205-5p的靶基因采用生物信息学分析预测。分别使用RT-qPCR的和Western印迹分析检测到下列的miR-205-5p抑制的候选靶基因水平和蛋白质的mRNA的表达。结果表明,A549细胞的相对存活率在的miR-205-5p的siRNA转染的细胞在24和48小时显著抑制与对照细胞相比。凋亡的所述miR-205-5p的siRNA的细胞中显着增加,与对照细胞相比。侵入细胞的以下的miR-205-5p的siRNA沉默数进行显著低于对照细胞相比。生物信息学分析表明,ERB-B2受体激酶3(erbB3的),锌指E框结合同源框2(ZEB2),网格蛋白重链(CLTC)和介体复合体亚基1(MED1)可以是的miR-205-的潜在靶基因5P。的miR-205-5p的表达降低显著增加ZEB2的mRNA和蛋白的表达,抑制erbB3的蛋白的表达,但对CLTC和MED1的表达水平没有显著影响。综上所述,通过ZEB2的上调和下调的ErbB3降低的miR-205-5p促进细胞凋亡和抑制增殖和侵袭的表达在肺癌A549细胞。目前的结果表明,增加的非小细胞肺癌组织中观察到的miR-205-5p表达可能有助于增殖增加和肺癌细胞的侵袭,从而癌症进展。

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