Promoter and histone methylation and p16(INK4A) gene expression in colon cancer.

Abstract:

: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.

journal_name

Exp Ther Med

authors

Yoruker EE,Mert U,Bugra D,Yamaner S,Dalay N

doi

10.3892/etm.2012.683

subject

Has Abstract

pub_date

2012-11-01 00:00:00

pages

865-870

issue

5

eissn

1792-0981

issn

1792-1015

pii

etm-04-05-0865

journal_volume

4

pub_type

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