Promoter and histone methylation and p16INK4A gene expression in colon cancer

被引:13
作者
Yoruker, Ebru Esin [1 ]
Mert, Ufuk [1 ]
Bugra, Dursun [2 ]
Yamaner, Sumer [2 ]
Dalay, Nejat [1 ]
机构
[1] Istanbul Univ, Inst Oncol, Dept Basic Oncol, TR-34093 Istanbul, Turkey
[2] Istanbul Univ, Istanbul Fac Med, Dept Surg, TR-34093 Istanbul, Turkey
关键词
colon cancer; epigenetics; gene expression; TUMOR-SUPPRESSOR GENE; DNA METHYLATION; P16; EXPRESSION; H3; METHYLATION; CLINICOPATHOLOGICAL FEATURES; COLORECTAL-CARCINOMA; HYPERMETHYLATION; MGMT; HETEROCHROMATIN; ADENOCARCINOMA;
D O I
10.3892/etm.2012.683
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
The inactivation of the cyclin-dependent kinase inhibitor p16(INK4A) gene by hypermethylation is observed in numerous types of cancer. New findings indicate that DNA and histone methylation act in concert in gene silencing. In this study, we investigated the methylation status of the p16(INK4A) gene promoter and the histone 3 lysine 9 residue in the tumors and matched normal tissue samples from patients with colorectal cancer and analyzed their association with gene expression. The methylation and expression of the p16(INK4A) gene were analyzed by real-time PCR, and histone methylation was analyzed by chromatin immunoprecipitation followed by real-time PCR. p16(INK4A) expression was significantly higher in the tumors compared to normal tissue. Mono-, di- and trimethylation levels of the H3K9 residue were similar in the tumor and normal tissue samples. We did not observe any significant correlation between p16(INK4A) methylation or expression and clinical parameters. Our results suggest that epigenetic modifications of the p16(INK4A) gene and histone lysine methylation do not play a major role in colon carcinogenesis.
引用
收藏
页码:865 / 870
页数:6
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