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Technol Cancer Res Treat ; 19: 1533033819892251, 2020.
Artículo en Inglés | MEDLINE | ID: mdl-31984860

RESUMEN

BACKGROUND: The incidence of nasopharyngeal carcinoma is increasing gradually, but the pathogenesis is not completely clear. MicroRNA, a highly conserved endogenous noncoding small molecule RNA, plays an essential role in the regulation of gene expression and is a hotspot in cancer research worldwide. OBJECTIVES: Although previous studies have confirmed that the abnormal expression of microRNAs is closely related to the progression of nasopharyngeal carcinoma, the role of miRNA-331-3p in nasopharyngeal carcinoma has not been studied. The purpose of this study was to explore the role and mechanism of miRNA-331-3p in the progression of nasopharyngeal carcinoma. MATERIALS AND METHODS: Real-time quantitative reverse transcription polymerase chain reaction was performed to detect the expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cell lines (CNE-1 and 5-8F cells). After overexpression of miRNA-331-3p in CNE-1 cells, cell proliferation was measured by Cell Counting Kit-8 assay, cell invasion was detected by Transwell assay, and apoptosis was tested by flow cytometry. In addition, the dual-luciferase reporter assay was used to identify the target gene of miRNA-331-3p and Western blotting was performed to measure the relative protein expression. RESULTS: The expression of miRNA-331-3p in nasopharyngeal carcinoma clinical samples and cells was decreased significantly. Overexpression of miRNA-331-3p markedly inhibited the proliferation and invasion of CNE-1 cells and promoted cell apoptosis. Moreover, overexpression of miRNA-331-3p reduced the expression of target gene elF4B, leading to inhibition of the phosphorylation of Phosphoinositide 3-kinase (PI3K) and Serine/ threonine kinase (AKT). CONCLUSION: miRNA-331-3p inhibited cell proliferation and induced cell apoptosis in nasopharyngeal carcinoma by targeting elF4B gene and then blocked the PI3K-AKT signaling pathway. SIGNIFICANCE: The role of miRNA-331-3p in the development of NPC and its mechanism provide new ideas for the treatment of nasopharyngeal carcinoma.


Asunto(s)
Apoptosis , Proliferación Celular , Fosfatidilinositol 3-Quinasa Clase I/antagonistas & inhibidores , Factores Eucarióticos de Iniciación/antagonistas & inhibidores , MicroARNs/genética , Carcinoma Nasofaríngeo/patología , Proteínas Proto-Oncogénicas c-akt/antagonistas & inhibidores , Línea Celular Tumoral , Movimiento Celular , Fosfatidilinositol 3-Quinasa Clase I/metabolismo , Factores Eucarióticos de Iniciación/metabolismo , Regulación Neoplásica de la Expresión Génica , Humanos , Carcinoma Nasofaríngeo/genética , Carcinoma Nasofaríngeo/metabolismo , Neoplasias Nasofaríngeas/genética , Neoplasias Nasofaríngeas/metabolismo , Neoplasias Nasofaríngeas/patología , Proteínas Proto-Oncogénicas c-akt/metabolismo , Transducción de Señal
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