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Promoter methylation status of the tumor suppressor gene SOX11 is associated with cell growth and invasion in nasopharyngeal carcinoma

BACKGROUND: The transcription factor SOX11 is one of members of the SRY box-containing (SOX) family emerging as important transcriptional regulators. In recent years, up-regulation of SOX11 has been detected in various types of solid tumors. In this study, the effects of promoter methylation of the...

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Autores principales: Zhang, Song, Li, Shuo, Gao, Jin-Liang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177000/
https://www.ncbi.nlm.nih.gov/pubmed/24188789
http://dx.doi.org/10.1186/1475-2867-13-109
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author Zhang, Song
Li, Shuo
Gao, Jin-Liang
author_facet Zhang, Song
Li, Shuo
Gao, Jin-Liang
author_sort Zhang, Song
collection PubMed
description BACKGROUND: The transcription factor SOX11 is one of members of the SRY box-containing (SOX) family emerging as important transcriptional regulators. In recent years, up-regulation of SOX11 has been detected in various types of solid tumors. In this study, the effects of promoter methylation of the SOX11 gene on SOX11 expression and cell growth and invasion of nasopharyngeal carcinoma were investigated. METHODS: In this study,methylation-specific PCR and real time quantitative PCR have been applied to investigate the effect of promoter methylation of the SOX11 gene on SOX11 expression in the nasopharyngeal carcinoma and chronic inflammation tissues. The nasopharyngeal carcinoma cell line (CNE2) was treated with 5-aza-2'-deoxycytidine. The effect of promoter methylation of SOX11 on growth and invasion of nasopharyngeal carcinoma cells was detected with MTT test and Boyden chamber Matrigel invasion assay. RESULTS: No or weak expression of SOX11 mRNA was detected in the nasopharyngeal carcinoma tissues of SOX11 gene promoter methylation. Strong expression of SOX11 mRNA was detected in the nasopharyngeal carcinoma tissues of SOX11 gene promoter unmethylation and chronic inflammation tissues of pharynx nasalis. SOX11 mRNA and protein were re-expressed, SOX11 gene was demethylated, and growth and invasion of cells were inhibited in CNE2 cell line after 5-aza-2'-deoxycytidine treatment. CONCLUSIONS: The results of the study indicate that expression of SOX11 mRNA and protein were related to SOX11 gene methylation status. SOX11 gene methylation may be plays a role in growth and invasion of nasopharyngeal carcinoma cells.
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spelling pubmed-41770002014-09-28 Promoter methylation status of the tumor suppressor gene SOX11 is associated with cell growth and invasion in nasopharyngeal carcinoma Zhang, Song Li, Shuo Gao, Jin-Liang Cancer Cell Int Primary Research BACKGROUND: The transcription factor SOX11 is one of members of the SRY box-containing (SOX) family emerging as important transcriptional regulators. In recent years, up-regulation of SOX11 has been detected in various types of solid tumors. In this study, the effects of promoter methylation of the SOX11 gene on SOX11 expression and cell growth and invasion of nasopharyngeal carcinoma were investigated. METHODS: In this study,methylation-specific PCR and real time quantitative PCR have been applied to investigate the effect of promoter methylation of the SOX11 gene on SOX11 expression in the nasopharyngeal carcinoma and chronic inflammation tissues. The nasopharyngeal carcinoma cell line (CNE2) was treated with 5-aza-2'-deoxycytidine. The effect of promoter methylation of SOX11 on growth and invasion of nasopharyngeal carcinoma cells was detected with MTT test and Boyden chamber Matrigel invasion assay. RESULTS: No or weak expression of SOX11 mRNA was detected in the nasopharyngeal carcinoma tissues of SOX11 gene promoter methylation. Strong expression of SOX11 mRNA was detected in the nasopharyngeal carcinoma tissues of SOX11 gene promoter unmethylation and chronic inflammation tissues of pharynx nasalis. SOX11 mRNA and protein were re-expressed, SOX11 gene was demethylated, and growth and invasion of cells were inhibited in CNE2 cell line after 5-aza-2'-deoxycytidine treatment. CONCLUSIONS: The results of the study indicate that expression of SOX11 mRNA and protein were related to SOX11 gene methylation status. SOX11 gene methylation may be plays a role in growth and invasion of nasopharyngeal carcinoma cells. BioMed Central 2013-11-05 /pmc/articles/PMC4177000/ /pubmed/24188789 http://dx.doi.org/10.1186/1475-2867-13-109 Text en Copyright © 2013 Zhang et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Primary Research
Zhang, Song
Li, Shuo
Gao, Jin-Liang
Promoter methylation status of the tumor suppressor gene SOX11 is associated with cell growth and invasion in nasopharyngeal carcinoma
title Promoter methylation status of the tumor suppressor gene SOX11 is associated with cell growth and invasion in nasopharyngeal carcinoma
title_full Promoter methylation status of the tumor suppressor gene SOX11 is associated with cell growth and invasion in nasopharyngeal carcinoma
title_fullStr Promoter methylation status of the tumor suppressor gene SOX11 is associated with cell growth and invasion in nasopharyngeal carcinoma
title_full_unstemmed Promoter methylation status of the tumor suppressor gene SOX11 is associated with cell growth and invasion in nasopharyngeal carcinoma
title_short Promoter methylation status of the tumor suppressor gene SOX11 is associated with cell growth and invasion in nasopharyngeal carcinoma
title_sort promoter methylation status of the tumor suppressor gene sox11 is associated with cell growth and invasion in nasopharyngeal carcinoma
topic Primary Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177000/
https://www.ncbi.nlm.nih.gov/pubmed/24188789
http://dx.doi.org/10.1186/1475-2867-13-109
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