구강 편평세포암에서 E-cadherin 유전자의 과메틸화
The hypermethylation of E-cadherin gene in oral squamous cell carcinoma
표성운, 김영실, 박지영, 김창현, 이원, 박민규,
소속 상세정보
표성운 ( Pyo Sung-Woon ) - 가톨릭대학교 의과대학 치과학교실 구강악안면외과
김영실 ( Kim Young-Sill ) - 제주대학교 의학전문대학원 병리학교실
박지영 ( Park Ji-Young ) - 가톨릭대학교 의과대학 치과학교실 구강악안면외과
김창현 ( Kim Chang-Hyun ) - 가톨릭대학교 의과대학 구강악안면외과학교실
이원 ( Lee Won ) - 가톨릭대학교 의과대학 치과학교실 구강악안면외과
박민규 ( Park Min-Kyu ) - 가톨릭대학교 의과대학 구강악안면외과학교실
KMID : 0355620080340020135
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.
키워드
Oral squamous cell carcinoma;E-cadherin;Hypermethylation;Methylation-specific PCR
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