Title of article :
Candidate tumor suppressor gene SLC5A8 is frequently down-regulated by promoter hypermethylation in prostate tumor
Author/Authors :
Park، نويسنده , , Jong Y. and Zheng، نويسنده , , Weipeng and Kim، نويسنده , , Donghwa and Cheng، نويسنده , , Jin Q. and Kumar، نويسنده , , Nagi and Ahmad، نويسنده , , Nazeel and Pow-Sang، نويسنده , , Julio، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2007
Pages :
7
From page :
359
To page :
365
Abstract :
Background ostate gland is the most common site of cancer and the third leading cause of cancer mortality in men. Solute carrier family 5 (iodide transporter), member 8 (SLC5A8) was proposed as a potential tumor suppressor gene which is silenced by epigenetic changes in various tumors. The aim of this study was to investigate the significance of DNA methylation in SLC5A8 expression in prostate tumors. s thylation status of the promoter region and expression of SLC5A8 were evaluated in prostate cancer cell lines, tumor and adjacent non-tumor prostate tissues from same prostate cancer patients, by using bisulphite-modified sequencing, RT-PCR and quantitative methylation-specific PCR (QMSP) analysis. s duced or lost expression of SLC5A8 was observed in 70% of the tumor tissues. The bisulphite-modified sequencing analysis on the prostate cancer cell lines which do not express SLC5A8 detected the densely methylated SLC5A8 promoter region. SLC5A8 was reactivated by treatment with DNA methyl transferase inhibitor, 5-azacytidine but not by trichostatin A (TSA). Higher methylation at the promoter region of SLC5A8 in primary prostate tumor tissues was detected as compared with those in adjacent non-tumor tissues (7/10, 70%). sions data suggested that DNA methylation in the SLC5A8 promoter region suppressed the expression of SLC5A8 in prostate tumor.
Keywords :
prostate cancer , DNA methylation , SLC5A8 , Tumor suppressor gene
Journal title :
Cancer Detection and Prevention
Serial Year :
2007
Journal title :
Cancer Detection and Prevention
Record number :
1835051
Link To Document :
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