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miR-144-3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the downregulation of the oncogenic gene, EZH2
Accumulating evidence demonstrates that microRNAs (miRNAs or miRs) play important roles in the development and progression of human malignancies, including oral squamous cell carcinoma (OSCC); however, the unique roles of miRNAs are not yet fully understood in OSCC. The present study aimed to identi...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7307824/ https://www.ncbi.nlm.nih.gov/pubmed/32626925 http://dx.doi.org/10.3892/ijmm.2020.4638 |
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author | He, Longlong Liao, Lifan Du, Liangzhi |
author_facet | He, Longlong Liao, Lifan Du, Liangzhi |
author_sort | He, Longlong |
collection | PubMed |
description | Accumulating evidence demonstrates that microRNAs (miRNAs or miRs) play important roles in the development and progression of human malignancies, including oral squamous cell carcinoma (OSCC); however, the unique roles of miRNAs are not yet fully understood in OSCC. The present study aimed to identify novel miRNAs associated with OSCC and to elucidate their functions. Based on a micro-array analysis, miR-144-3p was found to be one of the most significantly downregulated miRNAs in OSCC tissues. Its low expression was closely associated with tumor size, differentiation and lymph node metastasis. Functionally, miR-144-3p overexpression suppressed proliferation, promoted apoptosis, and suppressed the invasion and migration of OSCC cells. In addition, enhancer of zeste homolog 2 (EZH2), a well-known oncogene, was proven to be a direct target of miR-144-3p, and its protein expression was negatively regulated by miR-144-3p. Moreover, EZH2 expression was increased, and inversely correlated with the miR-144-3p level in OSCC tissues. Notably, EZH2 knockdown inhibited cell proliferation, promoted cell apoptosis, and suppressed the invasion and migration of OSCC cells, whereas EZH2 overexpression partially reversed the anticancer effects mediated by miR-144-3p overexpression. On the whole, the findings of the present study suggest that miR-144-3p functions as a tumor suppressor by targeting the EZH2 oncogene, and may thus be considered as a potential diagnostic and therapeutic target for OSCC. |
format | Online Article Text |
id | pubmed-7307824 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-73078242020-06-23 miR-144-3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the downregulation of the oncogenic gene, EZH2 He, Longlong Liao, Lifan Du, Liangzhi Int J Mol Med Articles Accumulating evidence demonstrates that microRNAs (miRNAs or miRs) play important roles in the development and progression of human malignancies, including oral squamous cell carcinoma (OSCC); however, the unique roles of miRNAs are not yet fully understood in OSCC. The present study aimed to identify novel miRNAs associated with OSCC and to elucidate their functions. Based on a micro-array analysis, miR-144-3p was found to be one of the most significantly downregulated miRNAs in OSCC tissues. Its low expression was closely associated with tumor size, differentiation and lymph node metastasis. Functionally, miR-144-3p overexpression suppressed proliferation, promoted apoptosis, and suppressed the invasion and migration of OSCC cells. In addition, enhancer of zeste homolog 2 (EZH2), a well-known oncogene, was proven to be a direct target of miR-144-3p, and its protein expression was negatively regulated by miR-144-3p. Moreover, EZH2 expression was increased, and inversely correlated with the miR-144-3p level in OSCC tissues. Notably, EZH2 knockdown inhibited cell proliferation, promoted cell apoptosis, and suppressed the invasion and migration of OSCC cells, whereas EZH2 overexpression partially reversed the anticancer effects mediated by miR-144-3p overexpression. On the whole, the findings of the present study suggest that miR-144-3p functions as a tumor suppressor by targeting the EZH2 oncogene, and may thus be considered as a potential diagnostic and therapeutic target for OSCC. D.A. Spandidos 2020-08 2020-06-11 /pmc/articles/PMC7307824/ /pubmed/32626925 http://dx.doi.org/10.3892/ijmm.2020.4638 Text en Copyright: © He et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles He, Longlong Liao, Lifan Du, Liangzhi miR-144-3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the downregulation of the oncogenic gene, EZH2 |
title | miR-144-3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the downregulation of the oncogenic gene, EZH2 |
title_full | miR-144-3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the downregulation of the oncogenic gene, EZH2 |
title_fullStr | miR-144-3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the downregulation of the oncogenic gene, EZH2 |
title_full_unstemmed | miR-144-3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the downregulation of the oncogenic gene, EZH2 |
title_short | miR-144-3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the downregulation of the oncogenic gene, EZH2 |
title_sort | mir-144-3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the downregulation of the oncogenic gene, ezh2 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7307824/ https://www.ncbi.nlm.nih.gov/pubmed/32626925 http://dx.doi.org/10.3892/ijmm.2020.4638 |
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