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MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway

BACKGROUND: Oral carcinoma, one of the most commonly diagnosed cancers, has a poor prognosis and low survival rate with treatment. In recent years, some studies reported the upregulation of miRNA-16 (miR-16) in the oral carcinoma, whereas some other studies confirmed the downregulation of miR-16. In...

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Autores principales: Liu, Lijun, Jiang, Han, Zhao, Jin, Wen, Hao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6112799/
https://www.ncbi.nlm.nih.gov/pubmed/30197522
http://dx.doi.org/10.2147/OTT.S153888
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author Liu, Lijun
Jiang, Han
Zhao, Jin
Wen, Hao
author_facet Liu, Lijun
Jiang, Han
Zhao, Jin
Wen, Hao
author_sort Liu, Lijun
collection PubMed
description BACKGROUND: Oral carcinoma, one of the most commonly diagnosed cancers, has a poor prognosis and low survival rate with treatment. In recent years, some studies reported the upregulation of miRNA-16 (miR-16) in the oral carcinoma, whereas some other studies confirmed the downregulation of miR-16. In the current study, we aimed to investigate the function of miR-16 in oral carcinoma. MATERIALS AND METHODS: Cell proliferation assay was measured by MTT assay, quantitative real time polymerase chain reaction (qRT-PCR) was used to evaluate the expression of miR-16, and apoptosis was analyzed by flow cytometry. In addition, the expression of proteins was detected by Western blot. Moreover, xenograft tumor model was established to detect the effect of miR-16 in vivo. RESULTS: The results suggested that miR-16 was downregulated in the oral carcinoma tissues. Overexpression of miR-16 inhibited the growth and proliferation of oral squamous carcinoma cells (OSCCs) and induced apoptosis both in vitro and in vivo, which is due to the suppression of Wnt/β-catenin signaling pathway. CONCLUSION: This study provides evidence that overexpression of miR-16 inhibits OSCC growth by regulating Wnt/β-catenin signaling. Our findings suggest that overexpression of miR-16 could be a potential approach for gene therapy of OSCC in future.
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spelling pubmed-61127992018-09-07 MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway Liu, Lijun Jiang, Han Zhao, Jin Wen, Hao Onco Targets Ther Original Research BACKGROUND: Oral carcinoma, one of the most commonly diagnosed cancers, has a poor prognosis and low survival rate with treatment. In recent years, some studies reported the upregulation of miRNA-16 (miR-16) in the oral carcinoma, whereas some other studies confirmed the downregulation of miR-16. In the current study, we aimed to investigate the function of miR-16 in oral carcinoma. MATERIALS AND METHODS: Cell proliferation assay was measured by MTT assay, quantitative real time polymerase chain reaction (qRT-PCR) was used to evaluate the expression of miR-16, and apoptosis was analyzed by flow cytometry. In addition, the expression of proteins was detected by Western blot. Moreover, xenograft tumor model was established to detect the effect of miR-16 in vivo. RESULTS: The results suggested that miR-16 was downregulated in the oral carcinoma tissues. Overexpression of miR-16 inhibited the growth and proliferation of oral squamous carcinoma cells (OSCCs) and induced apoptosis both in vitro and in vivo, which is due to the suppression of Wnt/β-catenin signaling pathway. CONCLUSION: This study provides evidence that overexpression of miR-16 inhibits OSCC growth by regulating Wnt/β-catenin signaling. Our findings suggest that overexpression of miR-16 could be a potential approach for gene therapy of OSCC in future. Dove Medical Press 2018-08-23 /pmc/articles/PMC6112799/ /pubmed/30197522 http://dx.doi.org/10.2147/OTT.S153888 Text en © 2018 Liu et al. This work is published and licensed by Dove Medical Press Limited The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License (http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.
spellingShingle Original Research
Liu, Lijun
Jiang, Han
Zhao, Jin
Wen, Hao
MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway
title MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway
title_full MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway
title_fullStr MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway
title_full_unstemmed MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway
title_short MiRNA-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing Wnt/β-catenin signaling pathway
title_sort mirna-16 inhibited oral squamous carcinoma tumor growth in vitro and in vivo via suppressing wnt/β-catenin signaling pathway
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6112799/
https://www.ncbi.nlm.nih.gov/pubmed/30197522
http://dx.doi.org/10.2147/OTT.S153888
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