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microRNA‐148a‐3p inhibited the proliferation and epithelial–mesenchymal transition progression of non‐small‐cell lung cancer via modulating Ras/MAPK/Erk signaling
Author(s) -
Xie Qiong,
Yu Zipu,
Lu Yuan,
Fan Jingya,
Ni Yiming,
Ma Liang
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.27899
Subject(s) - mapk/erk pathway , microrna , epithelial–mesenchymal transition , cell growth , microbiology and biotechnology , cancer research , signal transduction , biology , mesenchymal stem cell , cell , cancer , metastasis , gene , biochemistry , genetics
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.