DNA Methylation and Cancer Development: Molecular Mechanism

DNA methylation is a significant regulator of gene expression, and its role in carcinogenesis recently has been a subject of remarkable interest. The aim of this review is to analyze the mechanism and cell regulatory effects of both hypo- and hyper-DNA methylation on cancer. In this review, we repor...

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Published inCell biochemistry and biophysics Vol. 67; no. 2; pp. 501 - 513
Main Authors Akhavan-Niaki, Haleh, Samadani, Ali Akbar
Format Journal Article
LanguageEnglish
Published Boston Springer US 01.11.2013
Springer Nature B.V
Subjects
Animals
Biochemistry
Biological and Medical Physics
Biomedical and Life Sciences
Biophysics
Biotechnology
Carcinogenesis
Cell Biology
Deoxyribonucleic acid
DNA
DNA Methylation
Folic Acid - metabolism
Histones - metabolism
Humans
Life Sciences
Mutation
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Oxidative stress
Pharmacology/Toxicology
Review Paper
DNA methylation
Epigenetics
Oncogenesis
Histone modification
MicroRNA
Cancer
Online AccessGet full text

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Abstract DNA methylation is a significant regulator of gene expression, and its role in carcinogenesis recently has been a subject of remarkable interest. The aim of this review is to analyze the mechanism and cell regulatory effects of both hypo- and hyper-DNA methylation on cancer. In this review, we report new developments and their implications regarding the effects of DNA methylation on cancer development. Indeed, alteration of the pattern of DNA methylation has been a constant finding in cancer cells of the same type and differences in the pattern of DNA methylation not only occur in a variety of tumor types, but also in developmental processes Furthermore, the pattern of histone modification appears to be a predicator of the risk of recurrence of human cancers. It is well known that hypermethylation represses transcription of the promoter sections of tumor-suppressor genes leading to gene silencing. However, hypomethylation also has been identified as a cause of oncogenesis. Furthermore, experiments concerning the mechanism of methylation and its control have led to the discovery of many regulatory enzymes and proteins. This review reports on methods developed for the detection of 5-hydroxymethylcytosine methylation at the 5-methylcytosine of protein domains in the CpG context compared to non-methylated DNA, histone modification, and microRNA change.
AbstractList DNA methylation is a significant regulator of gene expression, and its role in carcinogenesis recently has been a subject of remarkable interest. The aim of this review is to analyze the mechanism and cell regulatory effects of both hypo- and hyper-DNA methylation on cancer. In this review, we report new developments and their implications regarding the effects of DNA methylation on cancer development. Indeed, alteration of the pattern of DNA methylation has been a constant finding in cancer cells of the same type and differences in the pattern of DNA methylation not only occur in a variety of tumor types, but also in developmental processes Furthermore, the pattern of histone modification appears to be a predicator of the risk of recurrence of human cancers. It is well known that hypermethylation represses transcription of the promoter sections of tumor-suppressor genes leading to gene silencing. However, hypomethylation also has been identified as a cause of oncogenesis. Furthermore, experiments concerning the mechanism of methylation and its control have led to the discovery of many regulatory enzymes and proteins. This review reports on methods developed for the detection of 5-hydroxymethylcytosine methylation at the 5-methylcytosine of protein domains in the CpG context compared to non-methylated DNA, histone modification, and microRNA change.
DNA methylation is a significant regulator of gene expression, and its role in carcinogenesis recently has been a subject of remarkable interest. The aim of this review is to analyze the mechanism and cell regulatory effects of both hypo- and hyper-DNA methylation on cancer. In this review, we report new developments and their implications regarding the effects of DNA methylation on cancer development. Indeed, alteration of the pattern of DNA methylation has been a constant finding in cancer cells of the same type and differences in the pattern of DNA methylation not only occur in a variety of tumor types, but also in developmental processes Furthermore, the pattern of histone modification appears to be a predicator of the risk of recurrence of human cancers. It is well known that hypermethylation represses transcription of the promoter sections of tumor-suppressor genes leading to gene silencing. However, hypomethylation also has been identified as a cause of oncogenesis. Furthermore, experiments concerning the mechanism of methylation and its control have led to the discovery of many regulatory enzymes and proteins. This review reports on methods developed for the detection of 5-hydroxymethylcytosine methylation at the 5-methylcytosine of protein domains in the CpG context compared to non-methylated DNA, histone modification, and microRNA change.DNA methylation is a significant regulator of gene expression, and its role in carcinogenesis recently has been a subject of remarkable interest. The aim of this review is to analyze the mechanism and cell regulatory effects of both hypo- and hyper-DNA methylation on cancer. In this review, we report new developments and their implications regarding the effects of DNA methylation on cancer development. Indeed, alteration of the pattern of DNA methylation has been a constant finding in cancer cells of the same type and differences in the pattern of DNA methylation not only occur in a variety of tumor types, but also in developmental processes Furthermore, the pattern of histone modification appears to be a predicator of the risk of recurrence of human cancers. It is well known that hypermethylation represses transcription of the promoter sections of tumor-suppressor genes leading to gene silencing. However, hypomethylation also has been identified as a cause of oncogenesis. Furthermore, experiments concerning the mechanism of methylation and its control have led to the discovery of many regulatory enzymes and proteins. This review reports on methods developed for the detection of 5-hydroxymethylcytosine methylation at the 5-methylcytosine of protein domains in the CpG context compared to non-methylated DNA, histone modification, and microRNA change.
Issue Title: Special Issue: Oxidative Stress in Health and Disease; Guest Editors: Hari S. Sharma, Vijay Kumar Kutala and Periannan Kuppusamy. Also Featuring: Regular Papers DNA methylation is a significant regulator of gene expression, and its role in carcinogenesis recently has been a subject of remarkable interest. The aim of this review is to analyze the mechanism and cell regulatory effects of both hypo- and hyper-DNA methylation on cancer. In this review, we report new developments and their implications regarding the effects of DNA methylation on cancer development. Indeed, alteration of the pattern of DNA methylation has been a constant finding in cancer cells of the same type and differences in the pattern of DNA methylation not only occur in a variety of tumor types, but also in developmental processes Furthermore, the pattern of histone modification appears to be a predicator of the risk of recurrence of human cancers. It is well known that hypermethylation represses transcription of the promoter sections of tumor-suppressor genes leading to gene silencing. However, hypomethylation also has been identified as a cause of oncogenesis. Furthermore, experiments concerning the mechanism of methylation and its control have led to the discovery of many regulatory enzymes and proteins. This review reports on methods developed for the detection of 5-hydroxymethylcytosine methylation at the 5-methylcytosine of protein domains in the CpG context compared to non-methylated DNA, histone modification, and microRNA change.[PUBLICATION ABSTRACT]
Author Samadani, Ali Akbar
Akhavan-Niaki, Haleh
Author_xml – sequence: 1
  givenname: Haleh
  surname: Akhavan-Niaki
  fullname: Akhavan-Niaki, Haleh
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– sequence: 2
  givenname: Ali Akbar
  surname: Samadani
  fullname: Samadani, Ali Akbar
  email: a_a_hormoz@yahoo.com
  organization: Cellular and Molecular Biology Research Center, Babol University of Medical Sciences
BackLink https://www.ncbi.nlm.nih.gov/pubmed/23508887$$D View this record in MEDLINE/PubMed
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ISSN 1085-9195
1559-0283
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IsPeerReviewed true
IsScholarly true
Issue 2
Keywords DNA methylation
Epigenetics
Oncogenesis
Histone modification
MicroRNA
Cancer
Language English
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crossref_primary_10_1007_s12013_013_9555_2
crossref_citationtrail_10_1007_s12013_013_9555_2
springer_journals_10_1007_s12013_013_9555_2
PublicationCentury 2000
PublicationDate 2013-11-01
PublicationDateYYYYMMDD 2013-11-01
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  year: 2013
  text: 2013-11-01
  day: 01
PublicationDecade 2010
PublicationPlace Boston
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PublicationTitle Cell biochemistry and biophysics
PublicationTitleAbbrev Cell Biochem Biophys
PublicationTitleAlternate Cell Biochem Biophys
PublicationYear 2013
Publisher Springer US
Springer Nature B.V
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Snippet DNA methylation is a significant regulator of gene expression, and its role in carcinogenesis recently has been a subject of remarkable interest. The aim of...
Issue Title: Special Issue: Oxidative Stress in Health and Disease; Guest Editors: Hari S. Sharma, Vijay Kumar Kutala and Periannan Kuppusamy. Also Featuring:...
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SubjectTerms Animals
Biochemistry
Biological and Medical Physics
Biomedical and Life Sciences
Biophysics
Biotechnology
Carcinogenesis
Cell Biology
Deoxyribonucleic acid
DNA
DNA Methylation
Folic Acid - metabolism
Histones - metabolism
Humans
Life Sciences
Mutation
Neoplasms - genetics
Neoplasms - metabolism
Neoplasms - pathology
Oxidative stress
Pharmacology/Toxicology
Review Paper
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Title DNA Methylation and Cancer Development: Molecular Mechanism
URI https://link.springer.com/article/10.1007/s12013-013-9555-2
https://www.ncbi.nlm.nih.gov/pubmed/23508887
https://www.proquest.com/docview/1446861012
https://www.proquest.com/docview/1447498855
https://www.proquest.com/docview/1496883229
Volume 67
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