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Clinical relevance of thyroid cell models in redox research
BACKGROUND: Thyroid-derived cell models are commonly used to investigate the characteristics of thyroid cancers. It is noteworthy that each in vitro single cell model system imitates only a few characteristics of thyroid cancer depending on e.g. source of cells or oncogene used to transform the cell...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4673788/ https://www.ncbi.nlm.nih.gov/pubmed/26664298 http://dx.doi.org/10.1186/s12935-015-0264-3 |
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author | Cammarota, Francesca Fiscardi, Francesco Esposito, Tiziana de Vita, Gabriella Salvatore, Marco Laukkanen, Mikko O. |
author_facet | Cammarota, Francesca Fiscardi, Francesco Esposito, Tiziana de Vita, Gabriella Salvatore, Marco Laukkanen, Mikko O. |
author_sort | Cammarota, Francesca |
collection | PubMed |
description | BACKGROUND: Thyroid-derived cell models are commonly used to investigate the characteristics of thyroid cancers. It is noteworthy that each in vitro single cell model system imitates only a few characteristics of thyroid cancer depending on e.g. source of cells or oncogene used to transform the cells. METHODS: In the current work we utilized rat thyroid cancer cell models to determine their clinical relevance in redox gene studies by comparing in vitro expression data to thyroid Oncomine microarray database. To survey the cell lines we analyzed mRNA expression of genes that produce superoxide anion (nox family), genes that catalyze destruction of superoxide anion to hydrogen peroxide (sod family), and genes that remove hydrogen peroxide from cellular environment (catalase, gpx family and prdx family). RESULTS: Based on the current results, rat thyroid PC Cl3, PC PTC1, PC E1A, or FRLT5 cell models can be used to study NOX2, NOX4, SOD2, SOD3, CATALASE, GPX1, GPX2, GPX5, PRDX2, and PRDX3 gene expression and function. CONCLUSIONS: Redox gene expression in rat originated single cell model systems used to study human thyroid carcinogenesis corresponds only partly with human redox gene expression, which may be caused by differences in redox gene activation stimulus. The data suggest careful estimation of the data observed in rat thyroid in vitro models. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12935-015-0264-3) contains supplementary material, which is available to authorized users. |
format | Online Article Text |
id | pubmed-4673788 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-46737882015-12-10 Clinical relevance of thyroid cell models in redox research Cammarota, Francesca Fiscardi, Francesco Esposito, Tiziana de Vita, Gabriella Salvatore, Marco Laukkanen, Mikko O. Cancer Cell Int Primary Research BACKGROUND: Thyroid-derived cell models are commonly used to investigate the characteristics of thyroid cancers. It is noteworthy that each in vitro single cell model system imitates only a few characteristics of thyroid cancer depending on e.g. source of cells or oncogene used to transform the cells. METHODS: In the current work we utilized rat thyroid cancer cell models to determine their clinical relevance in redox gene studies by comparing in vitro expression data to thyroid Oncomine microarray database. To survey the cell lines we analyzed mRNA expression of genes that produce superoxide anion (nox family), genes that catalyze destruction of superoxide anion to hydrogen peroxide (sod family), and genes that remove hydrogen peroxide from cellular environment (catalase, gpx family and prdx family). RESULTS: Based on the current results, rat thyroid PC Cl3, PC PTC1, PC E1A, or FRLT5 cell models can be used to study NOX2, NOX4, SOD2, SOD3, CATALASE, GPX1, GPX2, GPX5, PRDX2, and PRDX3 gene expression and function. CONCLUSIONS: Redox gene expression in rat originated single cell model systems used to study human thyroid carcinogenesis corresponds only partly with human redox gene expression, which may be caused by differences in redox gene activation stimulus. The data suggest careful estimation of the data observed in rat thyroid in vitro models. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12935-015-0264-3) contains supplementary material, which is available to authorized users. BioMed Central 2015-12-09 /pmc/articles/PMC4673788/ /pubmed/26664298 http://dx.doi.org/10.1186/s12935-015-0264-3 Text en © Cammarota et al. 2015 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Primary Research Cammarota, Francesca Fiscardi, Francesco Esposito, Tiziana de Vita, Gabriella Salvatore, Marco Laukkanen, Mikko O. Clinical relevance of thyroid cell models in redox research |
title | Clinical relevance of thyroid cell models in redox research |
title_full | Clinical relevance of thyroid cell models in redox research |
title_fullStr | Clinical relevance of thyroid cell models in redox research |
title_full_unstemmed | Clinical relevance of thyroid cell models in redox research |
title_short | Clinical relevance of thyroid cell models in redox research |
title_sort | clinical relevance of thyroid cell models in redox research |
topic | Primary Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4673788/ https://www.ncbi.nlm.nih.gov/pubmed/26664298 http://dx.doi.org/10.1186/s12935-015-0264-3 |
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