microRNA-148a-3p inhibited the proliferation and epithelial-mesenchymal transition progression of non-small-cell lung cancer via modulating Ras/MAPK/Erk signaling
microRNA-148a-3p inhibited the proliferation and epithelial-mesenchymal transition progression of non-small-cell lung cancer via modulating Ras/MAPK/Erk signaling
复制标题
microRNA-148a-3p通过调节Ras/MAPK/Erk信号抑制非小细胞肺癌的增殖和上皮间质转化进展
DOI：
10.1002/jcp.27899
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发表时间：
2019-08-01
影响因子：
5.6
通讯作者：
Ma, Liang
中科院分区：
文献类型：
--
作者：
Xie, Qiong;Yu, Zipu;Ma, Liang
SOS（Son of sevenless）是一种鸟嘌呤核苷酸交换因子，通过调控Ras的活化，调节丝裂原活化蛋白激酶/细胞外信号调节激酶信号通路。microRNA是基因表达的关键调节子，可作为肿瘤的生物标志物或治疗靶点。在这项研究中，我们发现miR-148 a-3 p在非小细胞肺癌（NSCLC）的发生和发展中起肿瘤抑制剂的作用。miR-148 a-3 p通过下调Ras激活的SOS 2表达抑制NSCLC细胞增殖和上皮-间质转化。我们的研究结果表明，miR-148 a-3 p可能在NSCLC包括K-Ras基因突变的肺癌中发挥重要作用，并通过靶向SOS 2发挥肿瘤抑制作用。因此，miR-148 a-3 p和SOS 2可能是开发更有用的NSCLC治疗方法的有效靶点。
Son of sevenless (SOS) is one of the guanine nucleotide exchange factors that can regulate the mitogen-activated protein kinase/extracellular signal regulated kinase signal pathway via controlling the activation of Ras. microRNAs are key regulon of gene expression and would be treated as tumor biomarkers or therapeutic targets. In this study, we find that miR-148a-3p acts as a tumor-suppressor in the development and progression of non-small-cell lung cancer (NSCLC). miR-148a-3p inhibits NSCLC cells proliferation and epithelial-mesenchymal transition by reducing the expression of SOS2, which refers Ras activating. Our findings demonstrate that the miR-148a-3p may play a significant role in NSCLC including the kind of lung cancer with K-Ras gene mutation, and it exerted the tumor inhibitor function by targeting SOS2. Because of that, miR-148a-3p and SOS2 may be an efficient target in developing more useful therapies against NSCLC.