Comparative analysis of methylation profiles in tissues of oral leukoplakia and oral squamous cell carcinoma
10.3760/cma.j.issn.1002-0098.2018.04.007
- VernacularTitle: 人口腔鳞状细胞癌和口腔白斑的基因甲基化谱分析
- Author:
Jie FU
1
,
2
;
Ying SU
3
;
Yao LIU
1
;
Xinyan ZHANG
3
Author Information
1. Department of Oral Medicine, Capital Medical University School of Stomatology, Beijing 100050, China
2. Institute of Dental Research, Capital Medical University School of Stomatology, Beijing 100050, China
3. Institute of Dental Research, Capital Medical University School of Stomatology, Beijing 100050, China
- Publication Type:Journal Article
- Keywords:
Carcinoma, squamous cell;
Leukoplakia, oral;
Methylation;
Epigenetics
- From:
Chinese Journal of Stomatology
2018;53(4):248-253
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To compare the methylation profiles in tissues of oral leukoplakia (OLK) and oral squamous cell carcinoma (OSCC) with healthy tissues of oral mucosa, in order to identify the role of DNA methylation played in tumorigenesis.
Methods:DNA samples extracted from tissues of 4 healthy oral mucosa, 4 OSCC and 4 OLK collected from patients of the Department of Oral Medicine, Capital Medical University School of Stomatology were examined and compared using Methylation 450 Bead Chip. The genes associated with differentially methylated CpG sites were selected for gene ontology (GO) analysis and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment.
Results:Multiple differentially methylated CpG sites were identified by using the above mentioned assay. Hypermethylation constitutes 86.18% (23 290/27 025) of methylation changes in OLK and hypomethylation accounts for 13.82% (3 734/27 025) of methylation changes. Both hypermethylated and hypomethylated CpG sites were markedly increased in OSCC tissue compared with OLK tissue. The majority of differentially methylated CpG sites were located outside CpG islands, with approximately one-fourth in CpG shores flanking the islands, which were considered highly important for gene regulation and tumorigenesis. Pathway analysis revealed that differentially methylated CpG sites in both OLK and OSCC patients shared the same pathway enrichments, most of which were correlated with carcinogenesis and cancer progression (e.g., DNA repair, cell cycle, and apoptosis).
Conclusions:In the present study, methylation-associated alterations affect almost all pathways in the cellular network in both OLK and OSCC. OLK and OSCC shared similar methylation changes whether in pathways or genes, indicating that epigenetically they might have the same molecular basis for disease progression.
