Promoter hypermethylation and silencing of CHFR mitotic stress checkpoint gene in human gastric cancers

被引:3
作者
Kang, HC
Kim, IJ
Park, JH
Shin, Y
Park, HW
Ku, JL
Yang, HK
Lee, KU
Choe, KJ
Park, JG
机构
[1] Natl Canc Ctr, Res Inst & Hosp, Goyang 411769, Gyeonggi, South Korea
[2] Seoul Natl Univ, Canc Res Inst, Korean Hereditary Tumor Registry, Seoul 110799, South Korea
[3] Seoul Natl Univ, Canc Res Inst, Seoul 110799, South Korea
[4] Seoul Natl Univ, Coll Med, Dept Surg, Seoul 110744, South Korea
关键词
CHFR; gastric cancer; promoter methylation; silencing;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
CHFR is a recently identified mitotic stress checkpoint gene. CHFR is ubiquitously expressed in normal human tissues, whereas loss of CHFR expression has been observed in human tumors. Silencing of CHFR has been associated with aberrant promoter methylation and histone deacetylation in several cancer types. In this study, we investigated epigenetic CHFR inactivation in human gastric cancers by examining CHFR expression and methylation status in gastric cancer cell lines with RT-PCR analysis, bisulfite PCR and sequencing. A series of primary gastric tumors were also analyzed for CHFR methylation. Eight of 12 (66.7%) gastric cancer cell lines and 19/43 (44.2%) primary gastric tumors showed CHFR methylation. In addition, CpG methylation status correlated well with CHFR expression in the human gastric cancer cell lines, in which treatment with 5-aza-dC resulted in de novo or enhanced expression of CHFR. Combination treatment of 5-aza-dC with trichostatin A showed a synergistic effect on CHFR expression in some cases. Our results indicate that aberrant promoter methylation of the CHFR gene was observed in a significant proportion of human gastric cancers and was responsible for the inactivation of the CHFR gene in gastric cancers.
引用
收藏
页码:129 / 133
页数:5
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