Abstract
Aberrant methylation of tumor suppressor genes has been reported as an important epigenetic silencer in head and neck cancer (HNC) pathogenesis. Here, we performed a comprehensive meta-analysis to evaluate the overall and specific impact of salivary gene promoter methylation on HNC risk. The methodological quality was assessed using the Newcastle–Ottawa scale (NOS). Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated to evaluate the strength of the association and Egger’s and Begg’s tests were applied to detect publication bias. The frequency of salivary DNA promoter methylation was significantly higher in HNC patients than in healthy controls (OR: 8.34 (95% CI = 6.10–11.39; p < 0.01). The pooled ORs showed a significant association between specific tumor-related genes and HNC risk: p16 (3.75; 95% CI = 2.51–5.60), MGMT (5.72; 95% CI = 3.00–10.91), DAPK (5.34; 95% CI = 2.18–13.10), TIMP3 (3.42; 95% CI = 1.99–5.88), and RASSF1A (7.69; 95% CI = 3.88–15.23). Overall, our meta-analysis provides precise evidence on the association between salivary DNA promoter hypermethylation and HNC risk. Thus, detection of promoter DNA methylation in saliva is a potential biomarker for predicting HNC risk.
Highlights
Aberrant DNA hypermethylation has been recognized as an important epigenetic Aberrant DNA hypermethylation has been recognized as an important epigen mechanism involved in head and neck carcinogenesis [1], suggesting its potential as a mechanism involved in head and neck carcinogenesis [1], suggesting its potential biomarker for evaluating cancer risk
Well-designed prospective clinical studies with large sample sizes are necessary to validate the results of this meta-analysis. The findings from this meta-analysis showed that salivary DNA promoter hypermethylation was associated with HNC risk
Salivary hypermethylation of p16, MGMT, death-associated protein kinase (DAPK), TIMP3, and RASSF1A showed an important role in HNC development
Summary
The important role of epigenetic mechanisms in carcinogenesis has been widely reported. Identification of specific genes that are altered by aberrant epigenetic processes contributes to better understanding molecular pathogenesis in HNC [1]. As one of the most important epigenetic alterations, DNA hypermethylation may lead to transcriptional silencing of tumor suppressor genes and, interfere in signaling pathways that control vital cell processes, such as DNA repair, apoptosis, cell proliferation, and cell-to-cell adhesion [2]. Gene promoter methylation is a common epigenetic event in early carcinogenesis, and represents a promising biomarker for high-risk group stratification, early cancer detection, and prognosis prediction [3]. Numerous studies have evaluated DNA methylation as a biomarker in a wide variety of tumors [4,5,6,7]. Hypermethylation of tumorrelated genes, such as cyclin-dependent kinase inhibitor 2A (CDKN2A), E-cadherin (CDH1), death-associated protein kinase (DAPK), phosphatase and tensin homolog (PTEN), and
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