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Effect of Physiological Levels of Sodium Selenite on the Expression and Regulation of Hypermethylated Tumor Supressor Gene in Human Breast Cancer Cell Line
Author(s) -
Chen YuHsin,
Yang Feili Lo,
Kao ChengFu,
Chen Yaling
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.916.6
Subject(s) - dna methylation , methylation , biology , dnmt1 , cancer research , cancer , tumor suppressor gene , breast cancer , methyltransferase , epigenetics , gene , gene expression , selenium , suppressor , medicine , carcinogenesis , genetics , chemistry , organic chemistry
Breast cancer (BC) was the 4th‐leading cause of cancer death in Taiwan with the rising incidence as malignant type in young premenopausal women during the recent decades. The aim of our study was to investigate the effects of physiological levels of selenite on regulation of BC tumor suppression gene through hypermethylation. Exposure of human breast cancer cell line MDA‐MB 231 to 1.5 and 2.5 μM of sodium selenite for 7 days significantly decreased cell invasion and migration ability compared to control. Selenite treatment (2.5 μM) reactivated the anti‐invasion gene CST6 (cystatin E/M), of which the promoter region hypomethylation was confirmed by methylation‐specific PCR. The protein expression of DNA methyltransferase £L (DMNT1) and histone deacetyl transferase I were also significantly decreased by selenite treatment. In conclusion, the suppressed invasion ability of MDA‐MB 231 cells by physiological levels of selenite may be due to the suppressed protein expression of DNMT1 as the result of reactivating the anti‐invasion genes such as CST6, of which the promoter region were hypomethylated. The results of this study are expected to explain the role of selenium in regulating the re‐expression of specific tumor suppressor genes and to be applied in improving the prognosis of breast cancer.(NSC98‐2320‐B‐030‐004) Grant Funding Source : NSC98‐2320‐B‐030‐004