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

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...

Descripción completa

Detalles Bibliográficos
Autores principales: YORUKER, EBRU ESIN, MERT, UFUK, BUGRA, DURSUN, YAMANER, SUMER, DALAY, NEJAT
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493785/
https://www.ncbi.nlm.nih.gov/pubmed/23226740
http://dx.doi.org/10.3892/etm.2012.683
_version_ 1782249327394029568
author YORUKER, EBRU ESIN
MERT, UFUK
BUGRA, DURSUN
YAMANER, SUMER
DALAY, NEJAT
author_facet YORUKER, EBRU ESIN
MERT, UFUK
BUGRA, DURSUN
YAMANER, SUMER
DALAY, NEJAT
author_sort YORUKER, EBRU ESIN
collection PubMed
description 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.
format Online
Article
Text
id pubmed-3493785
institution National Center for Biotechnology Information
language English
publishDate 2012
publisher D.A. Spandidos
record_format MEDLINE/PubMed
spelling pubmed-34937852012-12-06 Promoter and histone methylation and p16(INK4A) gene expression in colon cancer YORUKER, EBRU ESIN MERT, UFUK BUGRA, DURSUN YAMANER, SUMER DALAY, NEJAT Exp Ther Med Articles 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. D.A. Spandidos 2012-11 2012-08-24 /pmc/articles/PMC3493785/ /pubmed/23226740 http://dx.doi.org/10.3892/etm.2012.683 Text en Copyright © 2012, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Articles
YORUKER, EBRU ESIN
MERT, UFUK
BUGRA, DURSUN
YAMANER, SUMER
DALAY, NEJAT
Promoter and histone methylation and p16(INK4A) gene expression in colon cancer
title Promoter and histone methylation and p16(INK4A) gene expression in colon cancer
title_full Promoter and histone methylation and p16(INK4A) gene expression in colon cancer
title_fullStr Promoter and histone methylation and p16(INK4A) gene expression in colon cancer
title_full_unstemmed Promoter and histone methylation and p16(INK4A) gene expression in colon cancer
title_short Promoter and histone methylation and p16(INK4A) gene expression in colon cancer
title_sort promoter and histone methylation and p16(ink4a) gene expression in colon cancer
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3493785/
https://www.ncbi.nlm.nih.gov/pubmed/23226740
http://dx.doi.org/10.3892/etm.2012.683
work_keys_str_mv AT yorukerebruesin promoterandhistonemethylationandp16ink4ageneexpressionincoloncancer
AT mertufuk promoterandhistonemethylationandp16ink4ageneexpressionincoloncancer
AT bugradursun promoterandhistonemethylationandp16ink4ageneexpressionincoloncancer
AT yamanersumer promoterandhistonemethylationandp16ink4ageneexpressionincoloncancer
AT dalaynejat promoterandhistonemethylationandp16ink4ageneexpressionincoloncancer