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miR-592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin-dependent kinase 8
Medullary thyroid carcinoma (MTC) is a relatively rare subtype of thyroid cancer, accounting for 5–10% of all cases of thyroid cancer worldwide. Due to the current lack of knowledge regarding the tumorigenesis of MTC, the clinical treatment of MTC remains a challenge. It has been reported that micro...
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/PMC7453674/ https://www.ncbi.nlm.nih.gov/pubmed/32945439 http://dx.doi.org/10.3892/mmr.2020.11392 |
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author | Liu, Ting Meng, Jingjing Zhang, Yu |
author_facet | Liu, Ting Meng, Jingjing Zhang, Yu |
author_sort | Liu, Ting |
collection | PubMed |
description | Medullary thyroid carcinoma (MTC) is a relatively rare subtype of thyroid cancer, accounting for 5–10% of all cases of thyroid cancer worldwide. Due to the current lack of knowledge regarding the tumorigenesis of MTC, the clinical treatment of MTC remains a challenge. It has been reported that microRNAs (miRNAs) regulate the progression of MTC; however, the regulatory network of miRNAs and the exact underlying mechanisms are not completely understood. In the present study, an miRNA expression profile (GSE40807), consisting of 80 samples, was downloaded and analyzed using Gene Expression Omnibus-2R to identify differentially expressed miRNAs between MTC and normal samples. miR-592 expression levels were significantly increased in MTC tissues and cell lines compared with normal tissues and cell lines. Patients with high miR-592 expression levels exhibited a less favorable prognosis compared with patients with low miR-592 expression. The results suggested that miR-592 overexpression promoted TT and MZ-CRC-1 cell proliferation in vitro. In addition, miR-592 negatively regulated cyclin-dependent kinase 8 (CDK8) via targeted binding in MTC cells. Moreover, co-transfection of CDK8 overexpression plasmid and miR-592 mimic reversed miR-592-mediated MTC cell proliferation. In conclusion, miR-592 may serve as an oncogene in MTC by decreasing the expression of CDK8, indicating that the miR-592/CDK8 axis might serve as a promising therapeutic target for MTC. |
format | Online Article Text |
id | pubmed-7453674 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-74536742020-08-31 miR-592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin-dependent kinase 8 Liu, Ting Meng, Jingjing Zhang, Yu Mol Med Rep Articles Medullary thyroid carcinoma (MTC) is a relatively rare subtype of thyroid cancer, accounting for 5–10% of all cases of thyroid cancer worldwide. Due to the current lack of knowledge regarding the tumorigenesis of MTC, the clinical treatment of MTC remains a challenge. It has been reported that microRNAs (miRNAs) regulate the progression of MTC; however, the regulatory network of miRNAs and the exact underlying mechanisms are not completely understood. In the present study, an miRNA expression profile (GSE40807), consisting of 80 samples, was downloaded and analyzed using Gene Expression Omnibus-2R to identify differentially expressed miRNAs between MTC and normal samples. miR-592 expression levels were significantly increased in MTC tissues and cell lines compared with normal tissues and cell lines. Patients with high miR-592 expression levels exhibited a less favorable prognosis compared with patients with low miR-592 expression. The results suggested that miR-592 overexpression promoted TT and MZ-CRC-1 cell proliferation in vitro. In addition, miR-592 negatively regulated cyclin-dependent kinase 8 (CDK8) via targeted binding in MTC cells. Moreover, co-transfection of CDK8 overexpression plasmid and miR-592 mimic reversed miR-592-mediated MTC cell proliferation. In conclusion, miR-592 may serve as an oncogene in MTC by decreasing the expression of CDK8, indicating that the miR-592/CDK8 axis might serve as a promising therapeutic target for MTC. D.A. Spandidos 2020-10 2020-07-30 /pmc/articles/PMC7453674/ /pubmed/32945439 http://dx.doi.org/10.3892/mmr.2020.11392 Text en Copyright: © Liu 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 Liu, Ting Meng, Jingjing Zhang, Yu miR-592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin-dependent kinase 8 |
title | miR-592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin-dependent kinase 8 |
title_full | miR-592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin-dependent kinase 8 |
title_fullStr | miR-592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin-dependent kinase 8 |
title_full_unstemmed | miR-592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin-dependent kinase 8 |
title_short | miR-592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin-dependent kinase 8 |
title_sort | mir-592 acts as an oncogene and promotes medullary thyroid cancer tumorigenesis by targeting cyclin-dependent kinase 8 |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7453674/ https://www.ncbi.nlm.nih.gov/pubmed/32945439 http://dx.doi.org/10.3892/mmr.2020.11392 |
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