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首页> 外文期刊>Saudi Journal of Biological Sciences >MicroRNA-567 inhibits cell proliferation and induces cell apoptosis in A549 NSCLC cells by regulating cyclin-dependent kinase 8
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MicroRNA-567 inhibits cell proliferation and induces cell apoptosis in A549 NSCLC cells by regulating cyclin-dependent kinase 8

机译:通过调节细胞周期蛋白依赖性激酶8,MicroRNA-567抑制细胞增殖和诱导细胞凋亡和细胞凋亡

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MicroRNA-567 (miR-567) plays a decisive role in cancers whereas its role in non-small cell lung cancer (NSCLC) is still unexplored. This study was therefore planned to explore the regulatory function of miR-567 in A549 NSCLC cells and investigate its possible molecular mechanism that may help in NSCLC treatment. In the current study, miR-567 expression was examined by quantitative real time-polymerase chain reaction (qRT-PCR) in different NSCLC cell lines in addition to normal cell line. A549 NSCLC cells were transfected by miR-567 mimic, miR-567 inhibitor, and negative control siRNA. Cell proliferation was evaluated by MTT and 5-bromo-2′deoxyuridine assays. Cell cycle distribution and apoptosis were studied by flow cytometry. Bioinformatics analysis programs were used to expect the putative target of miR-567. The expression of cyclin-dependent kinase 8 (CDK8) gene at mRNA and protein levels were evaluated by using qRT-PCR and western blotting. Our results found that miR-567 expressions decreased in all the studied NSCLC cells as compared to the normal cell line. A549 cell proliferation was suppressed by miR-567 upregulation while cell apoptosis was promoted. Also, miR-567 upregulation induced cell cycle arrest at sub-G1 and S phases. CDK8 was expected as a target gene of miR-567. MiR-567 upregulation decreased CDK8 mRNA and protein expression while the downregulation of miR-567 increased CDK8 gene expression. These findings revealed that miR-567 may be a tumor suppressor in A549 NSCLC cells through regulating CDK8 gene expression and may serve as a novel therapeutic target for NSCLC treatment.
机译:MicroRNA-567(MiR-567)在癌症中起着决定性作用,而其在非小细胞肺癌(NSCLC)中的作用仍然是未开发的。因此,本研究计划探讨MIR-567在A549 NSCLC细胞中的调节功能,并调查其可能有助于NSCLC治疗的可能分子机制。在目前的研究中,除了正常细胞系之外,通过不同的NMSCLC细胞系中的定量实时聚合酶链反应(QRT-PCR)检查miR-567表达。通过MiR-567模拟,miR-567抑制剂和阴性对照siRNA转染A549 NSCLC细胞。通过MTT和5-溴-2'Deoxyuridine测定评估细胞增殖。通过流式细胞术研究细胞周期分布和细胞凋亡。生物信息学分析计划用于期望MIR-567的推定目标。通过使用QRT-PCR和Western印迹评估细胞周期蛋白依赖性激酶8(CDK8)基因的表达和蛋白质水平。我们的结果发现,与正常细胞系相比,MIR-567表达在所有研究的NSCLC细胞中减少。 MiR-567上调抑制了A549细胞增殖,而细胞凋亡促进。此外,miR-567上调诱导诱导亚g1和s阶段的细胞循环骤停。预计CDK8是MIR-567的靶基因。 miR-567 Upregulation降低了CDK8 mRNA和蛋白质表达,而MIR-567的下调增加了CDK8基因表达。这些发现显示MIR-567可以通过调节CDK8基因表达,作为A549 NSCLC细胞中的肿瘤抑制剂,并可作为NSCLC处理的新疗法。

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