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Abstract
BackgroundThe p16INK4a is an important tumor suppressor gene (TSG) and aberrant methylation of promoter is known to be a major inactivation mechanism of the tumor suppressor and tumor-related genes. Aberrant TSG methylation was considered an important epigenetic silencing mechanism in the progression of head and neck squamous cell carcinoma (HNSCC). However, some studies have reported differences in the methylation frequencies of P16INK4a promoter between cancer and the corresponding control group. Therefore, we conducted a meta-analysis to better identify the association.MethodsPubMed, Ovid, ISI Web of Science, and EMBASE were searched to identify eligible studies to evaluate the association of p16INK4a promoter methylation and HNSCC. Odds ratio (ORs) and 95% confidence intervals (95%CI) were calculated to evaluate the strength of association between p16INK4a promoter methylation and HNSCC.ResultsA total of twenty-one studies with 1155 cases and 1017 controls were included in the meta-analysis. The frequencies of p16INK4a promoter methylation in the cancer group were significantly higher than those in the control group (cancer group: median: 46.67%, range = 7.84%-95.12%; control group: median: 18.37%, range = 0–83.33%; respectively). The pooled odds ratio was 3.37 (95%CI = 2.32–4.90) in the cancer group versus the corresponding control group under the random-effects model.ConclusionThis meta-analysis of 21 published studies identified that aberrant methylation of p16INK4a promoter was found to be significantly associated with HNSCC.
Highlights
Head and neck squamous cell carcinoma (HNSCC) occurs in the oral cavity, oropharynx, hypopharynx and larynx
P16INK4a Promoter Methylation and HNSCC. This meta-analysis of 21 published studies identified that aberrant methylation of p16INK4a promoter was found to be significantly associated with HNSCC
P16 prevents the inactivation of retinoblastoma (Rb) protein by inhibiting the cyclin dependent kinases (CDks) and retinoblastoma (Rb) pathway plays an important role in apoptosis and cell cycle regulation [8]
Summary
Head and neck squamous cell carcinoma (HNSCC) occurs in the oral cavity, oropharynx, hypopharynx and larynx. The p16INK4a gene plays a key role in cell cycle regulation and is located on chromosome 9p21 which consisting of three exons and two introns, spanning approximately 8.5 kb [4, 5]. It is one of the most frequently altered genes observed in various human tumors [6, 7]. The p16INK4a is an important tumor suppressor gene (TSG) and aberrant methylation of promoter is known to be a major inactivation mechanism of the tumor suppressor and tumor-related genes. Aberrant TSG methylation was considered an important epigenetic silencing mechanism in the progression of head and neck squamous cell carcinoma (HNSCC). We conducted a meta-analysis to better identify the association
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