High-risk oral leukoplakia is associated with aberrant promoter methylation of multiple genesReport as inadecuate

High-risk oral leukoplakia is associated with aberrant promoter methylation of multiple genes - Download this document for free, or read online. Document in PDF available to download.

BMC Cancer

, 16:350

Genetics, genomics and epigenetics


BackgroundEarly detection of oral squamous cell carcinomas OSCCs is urgently needed to improve the prognosis and quality of life QOL of patients. Oral leukoplakias OLs, known as the most common premalignant lesions in the oral cavity, often precede OSCCs. Especially, OLs with dysplasia are known to have a high risk of malignant transformation. Here, we searched for the promoter methylation characteristic of high-risk OLs.

MethodsTo identify methylation-silenced genes, a combined analysis of methylated DNA immunoprecipitation MeDIP − CpG island CGI microarray analysis and expression microarray analysis after treatment with a demethylating agent was performed in two OSCC cell lines Ca9–22 and HSC-2. The methylation statuses of each gene were examined by methylation-specific PCR.

ResultsA total of 52 genes were identified as candidates for methylation-silenced genes in Ca9-22 or HSC-2. The promoter regions of 13 genes among the 15 genes randomly selected for further analysis were confirmed to be methylated in one or more of five cell lines. In OSCC tissues n = 26, 8 of the 13 genes, TSPYL5, EGFLAM, CLDN11, NKX2-3, RBP4, CMTM3, TRPC4, and MAP6, were methylated. In OL tissues n = 24, seven of the eight genes, except for EGFLAM, were found to be methylated in their promoter regions. There were significantly greater numbers of methylated genes in OLs with dysplasia than in those without dysplasia p < 0.0001.

ConclusionsOLs at high risk for malignant transformation were associated with aberrant promoter methylation of multiple genes.

KeywordsMethylation Promoter methylation Gene silencing Oral squamous cell carcinoma Oral leukoplakia Electronic supplementary materialThe online version of this article doi:10.1186-s12885-016-2371-5 contains supplementary material, which is available to authorized users.

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Author: Masanobu Abe - Satoshi Yamashita - Yoshiyuki Mori - Takahiro Abe - Hideto Saijo - Kazuto Hoshi - Toshikazu Ushijima - Tsuyo

Source: https://link.springer.com/

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