Involvement of CELSR3 Hypermethylation in Primary Oral Squamous Cell Carcinoma

Asian Pac J Cancer Prev. 2016;17(1):219-23. doi: 10.7314/apjcp.2016.17.1.219.

Abstract

Background: Promoter hypermethylation is a frequent epigenetic mechanism for gene transcription repression in cancer and is one of the hallmarks of the disease. Cadherin EGF LAG seven-pass G-type receptor 3 (CELSR3) contributes to cell contact-mediated communication. Dysregulation of promoter methylation has been reported in various cancers.

Objectives: The objectives of this study were to investigate the CELSR3 hypermethylation level in oral squamous cell carcinomas (OSCCs) using methylation-sensitive high-resolution melting analysis (MS-HRM) and to correlate CELSR3 methylation with patient demographic and clinicopathological parameters.

Materials and methods: Frozen tissue samples of healthy subjects' normal mucosa and OSCCs were examined with regard to their methylation levels of the CELSR3 gene using MS-HRM.

Results: MS-HRM analysis revealed a high methylation level of CELSR3 in 86% of OSCC cases. Significant correlations were found between CELSR3 quantitative methylation levels with patient ethnicity (P=0.005), age (P=0.024) and pathological stages (P=0.004). A moderate positive correlation between CELSR3 and patient age was also evident (R=0.444, P=0.001).

Conclusions: CELSR3 promoter hypermethylation may be an important mechanism involved in oral carcinogenesis. It may thus be used as a biomarker in OSCC prognostication.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Biomarkers, Tumor / genetics
  • Cadherins / genetics*
  • Carcinoma, Squamous Cell / genetics*
  • DNA Methylation / genetics*
  • DNA, Neoplasm / genetics
  • Female
  • Gene Expression Regulation, Neoplastic / genetics
  • Humans
  • Male
  • Middle Aged
  • Mouth Neoplasms / genetics*
  • Promoter Regions, Genetic / genetics
  • Receptors, Cell Surface / genetics*

Substances

  • Biomarkers, Tumor
  • Cadherins
  • Celsr3 protein, human
  • DNA, Neoplasm
  • Receptors, Cell Surface