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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...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2018
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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. |
format | Online Article Text |
id | pubmed-6112799 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
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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