E-cadherin promoter methylation and demethylation in epithelial ovarian carcinoma cells
10.3760/cma.j.issn.0529-567x.2009.07.014
- VernacularTitle:卵巢上皮性癌细胞中E钙黏素基因的甲基化状态及去甲基化的意义
- Author:
Pengpeng QU
;
Zheng SHI
;
Na LI
- Publication Type:Journal Article
- Keywords:
Ovarian neoplasms;
Cell line,tumor;
Cadherins;
Promoter regions(genetics);
Deoxycytidine;
Methylation
- From:
Chinese Journal of Obstetrics and Gynecology
2009;44(7):538-541
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the cytidylyl phosphate guanosine(CpG) islands methylation status of E-cadherin (E-cad) promoter region in human ovarian carcinoma cell lines (ES-2,3 AO, SKOV3 ), and the effect of 5-azacytidine-2 '-deoxycytidines (5-Aza-CdR ) on the cell proliferative ability, invasion and the expression of E-cad protein. Methods Methylation specific PCR(MSP) was used to detect CpG islands methylation status of E-cad promoter region in ES-2,3AO and SKOV3 cell lines. After treated with different concentrations of 5-Aza-CdR, morphological changes of cell lines were observed under microscope. The proliferative ability was evaluated by methyl thiazolyl tetrazolium(MTT) assay. E-cad protein expression was detected by western-blot and cellular invasion was investigated by 24-well matrigel invasion chambers. Results Hypermethylatian status of CpG islands of E-cad promoter region was observed in ES-2 and SKOV3 cell lines, but not in 3AO cell lines. After treated with 5-Aza-CdR (0.1,1.0,10.0 μmol/L), ES-2 and SKOV3 cell lines displayed morphological evidence of differentiation. 5-Aza-CdR was found to decrease proliferation as evidenced by cell growth curve , to increase the level of E-cad protein expression (P < 0.01 ), and effectively inhibit the ability of cell invasion(P <0.01 ). Conclusions CpG hypermethylation is an important mechanism of E-cad gene inactivation in ES-2 and SKOV3 cell lines. 5-Aza-CdR be found to inhibit proliferation and invasion, and increase the expression of E-cad probably by the inhibition of hypermethylation.