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MicroRNA‑133a downregulated EGFR expression in human non‑small cell lung cancer cells via AKT/ERK signaling
Author(s) -
Nannan Guo,
Yingnan Zhao,
Wei Zhang,
Shaojun Li,
Shanshan Li,
Jianqi Yu
Publication year - 2018
Publication title -
oncology letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.766
H-Index - 54
eISSN - 1792-1082
pISSN - 1792-1074
DOI - 10.3892/ol.2018.9399
Subject(s) - oncogene , protein kinase b , molecular medicine , microrna , cell cycle , cancer research , lung cancer , mapk/erk pathway , cancer , cell , biology , signal transduction , medicine , microbiology and biotechnology , oncology , gene , genetics
MicroRNAs (miRNAs) may serve important roles in the regulation of human non-small cell lung cancer (NSCLC) cell growth and apoptosis. To the best of our knowledge, the present study was the first to explore the role of miRNA-133a/epidermal growth factor receptor (EGFR) in regulating NSCLC cell growth and apoptosis via the AKT/extracellular signal-regulated kinase (ERK) signaling pathway. It was determined that miRNA-133a expression was lower in NSCLC tissue than in the adjacent mucosae. Additionally, EGFR expression in the NSCLC tissue was higher compared with in the adjacent mucosae. Furthermore, the upregulation of miRNA-133a in NSCLC cells suppressed cell growth and induced apoptosis. Upregulating miRNA-133a also increased caspase-3 protein expression, while suppressing that of EGFR, phosphorylated (p)-AKT and p-ERK in NSCLC cells. Therefore, the results of the current study demonstrated that miRNA-133a downregulates EGFR expression in NSCLC via the AKT/ERK signaling pathway. These findings provide insights into the function of miRNA-133a in NSCLC, as well as into the molecular mechanisms underlying the miRNA-133a-mediated downregulation of the EGFR/AKT/ERK signaling pathway in NSCLC.

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