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

• Published in: Diagnostic pathology 2016-01, Vol.11 (12), p.10-10, Article 10
• Main Authors: Shen, Zhisen, Chen, Xiaoying, Li, Qun, Zhou, Chongchang, Li, Jinyun, Ye, Huadan, Duan, Shiwei
• Format: Article
• Language: English
• Subjects: Adult; Age Factors; Aged; Aged, 80 and over; Biomarkers, Tumor - genetics; Carcinoma, Squamous Cell - genetics; Carcinoma, Squamous Cell - pathology; Care and treatment; Cell Differentiation; CpG Islands; Development and progression; Diagnosis; Disease Progression; DNA Methylation; Epigenesis, Genetic; Genetic aspects; Head and Neck Neoplasms - genetics; Head and Neck Neoplasms - pathology; Humans; Laryngeal Neoplasms - genetics; Laryngeal Neoplasms - pathology; Male; Methylation; Middle Aged; Multivariate Analysis; Neoplasm Staging; Promoter Regions, Genetic; Proportional Hazards Models; Receptors, Somatostatin - genetics; Risk Factors; Squamous cell carcinoma; Squamous Cell Carcinoma of Head and Neck
• ISSN: 1746-1596; 1746-1596
• DOI: 10.1186/s13000-016-0461-y

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. 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. 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). In conclusion, SSTR2 promoter hypermethylation might be associated with the risk and progression of LSCC in males.