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SSTR2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males

BACKGROUND: Somatostatin receptor 2 (SSTR2) encodes somatostatin receptor that can inhibit the cell proliferation of solid tumors. Promoter hypermethylation is likely to silence the expression of SSTR2. The goal of our study was to investigate the association between SSTR2 promoter methylation and t...

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Autores principales: Shen, Zhisen, Chen, Xiaoying, Li, Qun, Zhou, Chongchang, Li, Jinyun, Ye, Huadan, Duan, Shiwei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4722764/
https://www.ncbi.nlm.nih.gov/pubmed/26796520
http://dx.doi.org/10.1186/s13000-016-0461-y
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author Shen, Zhisen
Chen, Xiaoying
Li, Qun
Zhou, Chongchang
Li, Jinyun
Ye, Huadan
Duan, Shiwei
author_facet Shen, Zhisen
Chen, Xiaoying
Li, Qun
Zhou, Chongchang
Li, Jinyun
Ye, Huadan
Duan, Shiwei
author_sort Shen, Zhisen
collection PubMed
description BACKGROUND: Somatostatin receptor 2 (SSTR2) encodes somatostatin receptor that can inhibit the cell proliferation of solid tumors. Promoter hypermethylation is likely to silence the expression of SSTR2. The goal of our study was to investigate the association between SSTR2 promoter methylation and the risk and progression of laryngeal carcinoma. METHODS: In the current study, tumor tissues and their adjacent non-tumor tissues were collected from a total of 87 laryngeal squamous cell carcinoma (LSCC) male patients. DNA methylation levels of nine SSTR2 promoter CpGs were measured using the bisulphite pyrosequencing technology. RESULTS: Our results revealed that there was a significantly increased SSTR2 promoter methylation in LSCC tissues than in their adjacent non-cancerous tissues (adjusted P = 0.003). Breakdown analysis by age indicated that the significant association was mainly contributed by patients younger than 60 (adjusted P = 0.039) but not in patients older than 60. Meanwhile, the significant association was observed in the patients with moderately (adjusted P = 0.037) and well differentiated tissues (adjusted P = 0.028), as well as the patients with histological stage IV (adjusted P = 0.031). Multivariate Cox analysis suggested that SSTR2 promoter methylation was an independent prognostic factor of LSCC (HR = 1.127, 95 % CI = 1.034–1.228). CONCLUSIONS: In conclusion, SSTR2 promoter hypermethylation might be associated with the risk and progression of LSCC in males.
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spelling pubmed-47227642016-01-23 SSTR2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males Shen, Zhisen Chen, Xiaoying Li, Qun Zhou, Chongchang Li, Jinyun Ye, Huadan Duan, Shiwei Diagn Pathol Research BACKGROUND: Somatostatin receptor 2 (SSTR2) encodes somatostatin receptor that can inhibit the cell proliferation of solid tumors. Promoter hypermethylation is likely to silence the expression of SSTR2. The goal of our study was to investigate the association between SSTR2 promoter methylation and the risk and progression of laryngeal carcinoma. METHODS: In the current study, tumor tissues and their adjacent non-tumor tissues were collected from a total of 87 laryngeal squamous cell carcinoma (LSCC) male patients. DNA methylation levels of nine SSTR2 promoter CpGs were measured using the bisulphite pyrosequencing technology. RESULTS: Our results revealed that there was a significantly increased SSTR2 promoter methylation in LSCC tissues than in their adjacent non-cancerous tissues (adjusted P = 0.003). Breakdown analysis by age indicated that the significant association was mainly contributed by patients younger than 60 (adjusted P = 0.039) but not in patients older than 60. Meanwhile, the significant association was observed in the patients with moderately (adjusted P = 0.037) and well differentiated tissues (adjusted P = 0.028), as well as the patients with histological stage IV (adjusted P = 0.031). Multivariate Cox analysis suggested that SSTR2 promoter methylation was an independent prognostic factor of LSCC (HR = 1.127, 95 % CI = 1.034–1.228). CONCLUSIONS: In conclusion, SSTR2 promoter hypermethylation might be associated with the risk and progression of LSCC in males. BioMed Central 2016-01-22 /pmc/articles/PMC4722764/ /pubmed/26796520 http://dx.doi.org/10.1186/s13000-016-0461-y Text en © Shen et al. 2016 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 Research
Shen, Zhisen
Chen, Xiaoying
Li, Qun
Zhou, Chongchang
Li, Jinyun
Ye, Huadan
Duan, Shiwei
SSTR2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males
title SSTR2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males
title_full SSTR2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males
title_fullStr SSTR2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males
title_full_unstemmed SSTR2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males
title_short SSTR2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males
title_sort sstr2 promoter hypermethylation is associated with the risk and progression of laryngeal squamous cell carcinoma in males
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4722764/
https://www.ncbi.nlm.nih.gov/pubmed/26796520
http://dx.doi.org/10.1186/s13000-016-0461-y
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