The hypermethylation of E-cadherin gene in oral squamous cell carcinoma.
- Author:
Sung Woon PYO
1
;
Young Sill KIM
;
Ji Young PARK
;
Chang Hyen KIM
;
Won LEE
;
Min Kyu PARK
Author Information
1. Department of Oral and Maxillofacial Surgery, College of Medicine, The Catholic University of Korea. spyo@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Oral squamous cell carcinoma;
E-cadherin;
Hypermethylation;
Methylation-specific PCR
- MeSH:
Cadherins;
Carcinoma, Squamous Cell;
Dissociative Disorders;
Down-Regulation;
Hand;
Methylation;
Neoplasm Metastasis;
Polymerase Chain Reaction;
Promoter Regions, Genetic
- From:Journal of the Korean Association of Oral and Maxillofacial Surgeons
2008;34(2):135-140
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
Loss of E-cadherin (E-cad) expression has been found in multiple cancers and is postulated to facilitate tumor cell dissociation and metastais. Promotor methylation may provides an alternative pathway for loss of gene function. This study evaluated the role of hypermethylation in the down-regulation of E-cad in oral squamous cell carcinoma (OSCC). We examined the E-cad expression by immunohistochemical staining and detected methylation status by methylation-specific polymerase chain reaction (MSP) in 20 OSCC tissues. Overally, 12 (60 %) cases of hypermethylation of E-cad were detected and we found there were no correlation between methylation and age, histologic grade, lympn node metastasis, tumor size and clinical stage. However, Eleven (73.3 %) of 15 samples which was negative for E-cad staining showed hypermethylation of E-cad promotor region. On the other hand, only one (20 %) of 5 E-cad positive sample was observed with methylated status. The underexpression of E-cad was found to be related to promotor hypermethylation (p=0.035). In conclusion, we suggest that hypermethylation play a role in inactivation of E-cad gene and may be a appreciable biomarker for diagnosis and treatment of OSCC.
