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The miR-224 promotes non-small cell lung cancer cell proliferation by directly targeting RASSF8

机译:MiR-224通过直接靶向RASSF8促进非小细胞肺癌细胞增殖

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OBJECTIVE: The purpose of this study was to explore the mechanism of microRNA-224 (miR-224) in NSCLC. PATIENTS AND METHODS: Quantitative RT-PCR (qRT-PCR) was used to evaluate expression levels of miR-224. The association of miR-224 with the clinicopathologic features of NSCLC was evaluated in 56 patients. The roles of miR-224 in cell proliferation were analyzed in vivo and in vitro with pre-miR-224 transfected cells. Also, the regulation of RASSF8 by miR-224 was evaluated by qRT-PCR, Western blotting and luciferase reporter assays. RESULTS: In this study, we identified miR-224 to be significantly up-regulated in NSCLC tissues and associated with tumor size. Increased miR-224 expression promotes NSCLC cell proliferation by down-regulating RASSF8 at the mRNA and protein levels. The AKT pathway was found aberrantly activated after over-expression of miR-224. RASSF8 was identified as a direct target of miR-224 by bioinformatics analysis and luciferase reporter assay. CONCLUSIONS: The miR-224 played an oncogenic role in the proliferation of NSCLC by direct targeting RASSF8, and it is suggested that miR-224 may be a potential therapeutic target for NSCLC.
机译:目的:本研究的目的是探讨MicroRNA-224(MIR-224)在NSCLC中的机制。患者和方法:使用定量RT-PCR(QRT-PCR)来评估miR-224的表达水平。在56名患者中评估了miR-224与NSCLC临床病理特征的关联。 MiR-224在细胞增殖中的作用在体内和体外分析了MiR-224转染细胞。此外,通过QRT-PCR,Western印迹和荧光素酶报告器测定评估MiR-224的RASSF8的调节。结果:在本研究中,我们确定了MIR-224在NSCLC组织中显着上调并与肿瘤大小相关。增加的miR-224表达通过在mRNA和蛋白水平下调节rassf8来促进NSCLC细胞增殖。在MiR-224的过表达后发现AKT途径在异常激活。 RASSF8通过生物信息学分析和荧光素酶报告分析鉴定为MIR-224的直接靶标。结论:MIR-224通过直接靶向RASSF8在NSCLC的增殖中发挥了致癌作用,并且建议MIR-224可以是NSCLC的潜在治疗靶标。

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