Mechanism of loss of human esophageal cancer-related gene 4 (ECRG4) gene expression in esophageal squamous cell carcinoma cell line EC9706.
- Author:
Lin-Wei LI
1
;
Xi-Ying YU
;
Xiao-Yan LI
;
Li-Ping GUO
;
Yun ZHOU
;
Shi-Xin LU
Author Information
- Publication Type:Journal Article
- MeSH: Antimetabolites, Antineoplastic; pharmacology; Antineoplastic Agents; pharmacology; Arsenicals; pharmacology; Azacitidine; analogs & derivatives; pharmacology; Carcinoma, Squamous Cell; genetics; metabolism; pathology; Cell Line, Tumor; CpG Islands; genetics; DNA Methylation; Epigenesis, Genetic; Esophageal Neoplasms; genetics; metabolism; pathology; Exons; Gene Expression Regulation, Neoplastic; drug effects; Humans; Mutation; Neoplasm Proteins; genetics; metabolism; Oxides; pharmacology; Promoter Regions, Genetic; RNA, Messenger; metabolism
- From: Chinese Journal of Oncology 2011;33(8):570-573
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the mechanism of loss of human esophageal cancer-related gene 4 (ECRG4) expression in esophageal squamous cell carcinoma (ESCC.)
METHODSPCR-SSCP and DNA sequencing analysis were used to detect the mutation of ECRG4 exons in esophageal cancer and matched adjacent normal tissues of 80 patients. DNA bisulfite-modifying ssPCR sequencing assay was used to examine the methylation status of ECRG4 promoter in human esophageal squamous cell carcinoma EC9706 cells. The re-expression of ECRG4 mRNA was examined by RT-PCR in EC9706 cells, after treatment with either demethylation drug 5-aza-2'-deoxycytidine or arsenic trioxide.
RESULTSNo mutation in the four ECRG4 exons was found in all the ESCC and matched normal adjacent tissues. RT-PCR showed that 11 of 16 CpG islands of ECRG4 promoter were hypermethylated, while ECRG4 mRNA expression level was undetectable in the EC9706 cells. The ECRG4 mRNA was re-expressed after treatment with either demethylation drug 5-aza-2'-deoxycytidine or arsenic trioxide.
CONCLUSIONThe epigenetic mechanism of methylation is a reason of loss of ECRG4 gene expression in the ESCC cell line EC9706.