[Aberrant methylation of T-cadherin gene in human esophageal carcinoma cells].
OBJECTIVE
To explore the methylation status of T-cadherin promoter region in human esophageal carcinoma cell lines EC1 and EC109 and elucidate the effects of 5-azacytidine-2'-deoxycytidine (5-Aza-CdR) on their abilities of proliferation and invasion, the methylation status and the expression of T-cadherin.


METHODS
The expression level of T-cadherin was measured by Western blot. And the methylation status of T-cadherin promoter region was analyzed by methylation-specific PCR (polymerase chain reaction), separately before and after a treatment of demethylating agent 5-Aza-CdR.


RESULTS
The T-cadherin gene was hypermethylated in EC109 cells but semi-methylated in EC1 cells. After a treatment of 5-Aza-CdR, T-cadherin gene methylation was reversed. And the gene expression was strongly up-regulated in both cells. 5-Aza-CdR could decrease the proliferation and effectively inhibit the ability of cell invasion (P < 0.01).


CONCLUSIONS
The aberrant methylation in promoter region is an important mechanism of T-cadherin gene inactivation in human esophageal carcinoma cells. 5-Aza-CdR can increase the expression of T-cadherin by a reversal of hypermethylation and effectively inhibit the proliferation and invasion of tumor cells.
Department of Medicine & Radiation Oncology, First Affiliated Hospital, Wenzhou Medical College, Wenzhou 325000, China. jz96329@163.com
Zhao
Z
Jing
Chang-lin
CL
Zou
Gang
G
Li
Xia
X
Deng
Shi-xiu
SX
Wu
D001374:Azacitidine / Q000494:pharmacology; D015820:Cadherins / Q000235:genetics / Q000378:metabolism*; D045744:Cell Line, Tumor; D019175:DNA Methylation; D004938:Esophageal Neoplasms / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D011401:Promoter Regions, Genetic
D015820:Cadherins; D001374:Azacitidine