- Author:
Shuhong MING
1
;
Jing GAO
;
Tieying SUN
Author Information
- Publication Type:Journal Article
- MeSH: Azacitidine; analogs & derivatives; pharmacology; Cell Adhesion Molecule-1; Cell Adhesion Molecules; antagonists & inhibitors; genetics; Cell Line, Tumor; DNA Methylation; Gene Silencing; Humans; Immunoglobulins; genetics; Lung Neoplasms; genetics; pathology; Promoter Regions, Genetic; Tumor Suppressor Proteins; antagonists & inhibitors; genetics
- From: Chinese Journal of Lung Cancer 2010;13(5):464-469
- CountryChina
- Language:Chinese
-
Abstract:
BACKGROUND AND OBJECTIVEThe expression of TSLC1 is downregulated or abrogated in many kinds of tumors, and its downregulation is highly associated with DNA hypermethlyation. The aim of this study is to explore the relationship between TSLC1 silencing and DNA methylation of its promoter region in lung cancer cells.
METHODSWe detected the expression pattern of TSLC1 in human normal lung tissue and three lung cancer cell lines (A549, NCI-H446 and Calu-3) by semi-quantitative RT-PCR and Real-time PCR. Then we detected the status of DNA methylation in TSLC1 promoter region with bisulfite sequencing in above normal lung tissue and lung cancer cell lines. After treatment of above cell lines with the inhibitor of DNA methyltransferase 5-Aza-2-deoxycytidine (5-Aza-dC), we detected the expression change of TSLC1 by Real-time PCR before and after the treatment of 5-Aza-dC.
RESULTSThere was no methylation in TSLC1 promoter region in normal lung tissue and A549 cell line in which TSLC1 expressed; while there was DNA hypermethylation in TSLC1 promoter region in NCI-H446 and Calu-3 cell lines in which TSLC1 was abrogated, also the expression of TSLC1 in NCI-H446 and Calu-3 cell lines could be restored after treatment of 5-Aza-dC.
CONCLUSIONThe silencing of TSLC1 in lung cancer cells is due to the hypermethylation of its promoter region.