microRNA‐148a‐3p inhibited the proliferation and epithelial–mesenchymal transition progression of non‐small‐cell lung cancer via modulating Ras/MAPK/Erk signaling

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 bioma...

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Veröffentlicht in:Journal of cellular physiology 2019-08, Vol.234 (8), p.12786-12799
Hauptverfasser: Xie, Qiong, Yu, Zipu, Lu, Yuan, Fan, Jingya, Ni, Yiming, Ma, Liang
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container_end_page 12799
container_issue 8
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container_title Journal of cellular physiology
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creator Xie, Qiong
Yu, Zipu
Lu, Yuan
Fan, Jingya
Ni, Yiming
Ma, Liang
description 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. miR‐148a‐3p is downregulated in non‐small‐cell lung cancer (NSCLC) cells, and overexpression of miR‐148a‐3p inhibits the proliferation and the motility of NSCLC cells. miR‐148a‐3p inhibited the proliferation and epithelial–mesenchymal transition progression of NSCLC via targeting SOS2. SOS2 modulates Ras/MAPK/ERK signaling by controlling activation of Ras.
doi_str_mv 10.1002/jcp.27899
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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. miR‐148a‐3p is downregulated in non‐small‐cell lung cancer (NSCLC) cells, and overexpression of miR‐148a‐3p inhibits the proliferation and the motility of NSCLC cells. miR‐148a‐3p inhibited the proliferation and epithelial–mesenchymal transition progression of NSCLC via targeting SOS2. 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subjects Biomarkers
Biomarkers, Tumor - genetics
Cancer
Carcinoma, Non-Small-Cell Lung - genetics
Cell Movement - genetics
Cell proliferation
Cell Proliferation - genetics
Disease Progression
Epithelial-Mesenchymal Transition - genetics
epithelial–mesenchymal transition
Extracellular signal-regulated kinase
Gene expression
Gene Expression Regulation, Neoplastic - genetics
Guanine
Guanine nucleotide exchange factor
Humans
Kinases
Lung cancer
Lung Neoplasms - genetics
Lung Neoplasms - pathology
MAP kinase
Mesenchyme
MicroRNAs - genetics
miRNA
miR‐148a‐3p
Mitogen-Activated Protein Kinase Kinases - metabolism
Mutation
Non-small cell lung carcinoma
non‐small‐cell lung cancer
Point mutation
proliferation
Protein kinase
Proteins
Ras protein
Ribonucleic acid
RNA
Son of Sevenless Proteins - genetics
SOS2
Therapeutic applications
Tumors
title microRNA‐148a‐3p inhibited the proliferation and epithelial–mesenchymal transition progression of non‐small‐cell lung cancer via modulating Ras/MAPK/Erk signaling
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