DNA methylation in salivary adenoid cystic carcinoma cell lines.
- Author:
Chun-ye ZHANG
1
;
Xiao-jian ZHOU
;
Zhi-yuan ZHANG
;
Jiang LI
Author Information
- Publication Type:Journal Article
- MeSH: Cadherins; genetics; metabolism; Carcinoma, Adenoid Cystic; genetics; pathology; Cell Line, Tumor; Cyclin-Dependent Kinase Inhibitor p16; DNA Methylation; Humans; Neoplasm Proteins; genetics; metabolism; Promoter Regions, Genetic; genetics; Salivary Gland Neoplasms; genetics; pathology
- From: Chinese Journal of Stomatology 2007;42(3):135-139
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the promoter methylation status of tumor suppressor gene and the relationship between promoter methylation and mRNA, protein expression of tumor suppressor gene in salivary adenoid cystic carcinoma (ACC) cell lines.
METHODSPromoter methylation status of E-cad, p16, RASSF1A, DAPK, and MGMT was determined by methylation-specific polymerase chain reaction (MSP) in ACC cell lines, ACC-2, ACC-3, and ACC-M. E-cad, p16 protein and mRNA expression was also examined by IHC and RT-PCR in 3 ACC cell lines.
RESULTSAll the three salivary ACC cell lines exhibited E-cad, p16 promoter methylation, but no methylation of RASSF1A, DAPK, and MGMT was found. There was p16 protein and mRNA expression but no E-cad expression in 3 ACC cell lines.
CONCLUSIONSThe results suggest that in ACC cell lines, promoter methylation of E-cad, p16 is a common event, and promoter methylation may be one of the major mechanism for inactivation of E-cad.
