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MicroRNA meta-signature of oral cancer: evidence from a meta-analysis

AIM: It was the aim of the study to identify commonly deregulated miRNAs in oral cancer patients by performing a meta-analysis of previously published miRNA expression profiles in cancer and matched normal non-cancerous tissue in such patients. MATERIAL AND METHODS: Meta-analysis included seven inde...

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Detalles Bibliográficos
Autores principales: Zeljic, Katarina, Jovanovic, Ivan, Jovanovic, Jasmina, Magic, Zvonko, Stankovic, Aleksandra, Supic, Gordana
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Taylor & Francis 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5901467/
https://www.ncbi.nlm.nih.gov/pubmed/29482431
http://dx.doi.org/10.1080/03009734.2018.1439551
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author Zeljic, Katarina
Jovanovic, Ivan
Jovanovic, Jasmina
Magic, Zvonko
Stankovic, Aleksandra
Supic, Gordana
author_facet Zeljic, Katarina
Jovanovic, Ivan
Jovanovic, Jasmina
Magic, Zvonko
Stankovic, Aleksandra
Supic, Gordana
author_sort Zeljic, Katarina
collection PubMed
description AIM: It was the aim of the study to identify commonly deregulated miRNAs in oral cancer patients by performing a meta-analysis of previously published miRNA expression profiles in cancer and matched normal non-cancerous tissue in such patients. MATERIAL AND METHODS: Meta-analysis included seven independent studies analyzed by a vote-counting method followed by bioinformatic enrichment analysis. RESULTS: Amongst seven independent studies included in the meta-analysis, 20 miRNAs were found to be deregulated in oral cancer when compared with non-cancerous tissue. Eleven miRNAs were consistently up-regulated in three or more studies (miR-21-5p, miR-31-5p, miR-135b-5p, miR-31-3p, miR-93-5p, miR-34b-5p, miR-424-5p, miR-18a-5p, miR-455-3p, miR-450a-5p, miR-21-3p), and nine were down-regulated (miR-139-5p, miR-30a-3p, miR-376c-3p, miR-885-5p, miR-375, miR-486-5p, miR-411-5p, miR-133a-3p, miR-30a-5p). The meta-signature of identified miRNAs was functionally characterized by KEGG enrichment analysis. Twenty-four KEGG pathways were significantly enriched, and TGF-beta signaling was the most enriched signaling pathway. The highest number of meta-signature miRNAs was involved in the sphingolipid signaling pathway. Natural killer cell-mediated cytotoxicity was the pathway with most genes regulated by identified miRNAs. The rest of the enriched pathways in our miRNA list describe different malignancies and signaling. CONCLUSIONS: The identified miRNA meta-signature might be considered as a potential battery of biomarkers when distinguishing oral cancer tissue from normal, non-cancerous tissue. Further mechanistic studies are warranted in order to confirm and fully elucidate the role of deregulated miRNAs in oral cancer.
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spelling pubmed-59014672018-04-23 MicroRNA meta-signature of oral cancer: evidence from a meta-analysis Zeljic, Katarina Jovanovic, Ivan Jovanovic, Jasmina Magic, Zvonko Stankovic, Aleksandra Supic, Gordana Ups J Med Sci Articles AIM: It was the aim of the study to identify commonly deregulated miRNAs in oral cancer patients by performing a meta-analysis of previously published miRNA expression profiles in cancer and matched normal non-cancerous tissue in such patients. MATERIAL AND METHODS: Meta-analysis included seven independent studies analyzed by a vote-counting method followed by bioinformatic enrichment analysis. RESULTS: Amongst seven independent studies included in the meta-analysis, 20 miRNAs were found to be deregulated in oral cancer when compared with non-cancerous tissue. Eleven miRNAs were consistently up-regulated in three or more studies (miR-21-5p, miR-31-5p, miR-135b-5p, miR-31-3p, miR-93-5p, miR-34b-5p, miR-424-5p, miR-18a-5p, miR-455-3p, miR-450a-5p, miR-21-3p), and nine were down-regulated (miR-139-5p, miR-30a-3p, miR-376c-3p, miR-885-5p, miR-375, miR-486-5p, miR-411-5p, miR-133a-3p, miR-30a-5p). The meta-signature of identified miRNAs was functionally characterized by KEGG enrichment analysis. Twenty-four KEGG pathways were significantly enriched, and TGF-beta signaling was the most enriched signaling pathway. The highest number of meta-signature miRNAs was involved in the sphingolipid signaling pathway. Natural killer cell-mediated cytotoxicity was the pathway with most genes regulated by identified miRNAs. The rest of the enriched pathways in our miRNA list describe different malignancies and signaling. CONCLUSIONS: The identified miRNA meta-signature might be considered as a potential battery of biomarkers when distinguishing oral cancer tissue from normal, non-cancerous tissue. Further mechanistic studies are warranted in order to confirm and fully elucidate the role of deregulated miRNAs in oral cancer. Taylor & Francis 2018-03 2018-02-26 /pmc/articles/PMC5901467/ /pubmed/29482431 http://dx.doi.org/10.1080/03009734.2018.1439551 Text en © 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group. http://creativecommons.org/licenses/by/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Articles
Zeljic, Katarina
Jovanovic, Ivan
Jovanovic, Jasmina
Magic, Zvonko
Stankovic, Aleksandra
Supic, Gordana
MicroRNA meta-signature of oral cancer: evidence from a meta-analysis
title MicroRNA meta-signature of oral cancer: evidence from a meta-analysis
title_full MicroRNA meta-signature of oral cancer: evidence from a meta-analysis
title_fullStr MicroRNA meta-signature of oral cancer: evidence from a meta-analysis
title_full_unstemmed MicroRNA meta-signature of oral cancer: evidence from a meta-analysis
title_short MicroRNA meta-signature of oral cancer: evidence from a meta-analysis
title_sort microrna meta-signature of oral cancer: evidence from a meta-analysis
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5901467/
https://www.ncbi.nlm.nih.gov/pubmed/29482431
http://dx.doi.org/10.1080/03009734.2018.1439551
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