De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands

The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1 . Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this ha...

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Published inNature communications Vol. 12; no. 1; pp. 694 - 13
Main Authors Masalmeh, Roza H. Ali, Taglini, Francesca, Rubio-Ramon, Cristina, Musialik, Kamila I., Higham, Jonathan, Davidson-Smith, Hazel, Kafetzopoulos, Ioannis, Pawlicka, Kamila P., Finan, Hannah M., Clark, Richard, Wills, Jimi, Finch, Andrew J., Murphy, Lee, Sproul, Duncan
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 29.01.2021
Nature Publishing Group
Nature Portfolio
Subjects
38/1
38/109
38/15
38/22
38/77
631/208/176
631/208/177
631/337/176/1988
631/67/68/2486
692/4028/67/1504/1885
Aberration
Cancer
Carcinogenesis - genetics
Cell Line, Tumor
Chromatin Immunoprecipitation Sequencing
Colon
Colon - pathology
Colorectal cancer
Colorectal carcinoma
Colorectal Neoplasms - genetics
Colorectal Neoplasms - pathology
CpG islands
CpG Islands - genetics
Datasets as Topic
Deoxyribonucleic acid
DNA
DNA (Cytosine-5-)-Methyltransferases - genetics
DNA (Cytosine-5-)-Methyltransferases - metabolism
DNA Methylation
DNA methyltransferase
Elongation
Epigenesis, Genetic
Gene Expression Regulation, Neoplastic
Gene Knockout Techniques
Histone Code - genetics
Histones
Histones - genetics
Humanities and Social Sciences
Humans
Islands
MLH1 protein
multidisciplinary
Nucleotide sequence
Promoter Regions, Genetic - genetics
Science
Science (multidisciplinary)
Suppressors
Transcription elongation
Transcription, Genetic
Tumorigenesis
Tumors
Online AccessGet full text

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Abstract The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1 . Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis. Aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours. Here the authors use ectopically integrated CpG islands in colorectal cancer cells and find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation, and that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3.
AbstractList The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1 . Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis. Aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours. Here the authors use ectopically integrated CpG islands in colorectal cancer cells and find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation, and that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3.
Aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours. Here the authors use ectopically integrated CpG islands in colorectal cancer cells and find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation, and that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3.
The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.
The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.
The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1. Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.Aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours. Here the authors use ectopically integrated CpG islands in colorectal cancer cells and find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation, and that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3.
The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as MLH1 . Current models propose that these CpG islands are targeted by de novo DNA methyltransferases in a sequence-specific manner, but this has not been tested. Using ectopically integrated CpG islands, here we find that aberrantly methylated CpG islands are subject to low levels of de novo DNA methylation activity in colorectal cancer cells. By delineating DNA methyltransferase targets, we find that instead de novo DNA methylation activity is targeted primarily to CpG islands marked by the histone modification H3K36me3, a mark associated with transcriptional elongation. These H3K36me3 marked CpG islands are heavily methylated in colorectal tumours and the normal colon suggesting that de novo DNA methyltransferase activity at CpG islands in colorectal cancer is focused on similar targets to normal tissues and not greatly remodelled by tumourigenesis.
ArticleNumber 694
Author Sproul, Duncan
Pawlicka, Kamila P.
Finan, Hannah M.
Wills, Jimi
Kafetzopoulos, Ioannis
Musialik, Kamila I.
Davidson-Smith, Hazel
Finch, Andrew J.
Masalmeh, Roza H. Ali
Murphy, Lee
Clark, Richard
Rubio-Ramon, Cristina
Taglini, Francesca
Higham, Jonathan
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/33514701$$D View this record in MEDLINE/PubMed
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  publication-title: Bioinformatics
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Snippet The aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours and may silence the expression of tumour suppressors such as...
Aberrant gain of DNA methylation at CpG islands is frequently observed in colorectal tumours. Here the authors use ectopically integrated CpG islands in...
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StartPage 694
SubjectTerms 38/1
38/109
38/15
38/22
38/77
631/208/176
631/208/177
631/337/176/1988
631/67/68/2486
692/4028/67/1504/1885
Aberration
Cancer
Carcinogenesis - genetics
Cell Line, Tumor
Chromatin Immunoprecipitation Sequencing
Colon
Colon - pathology
Colorectal cancer
Colorectal carcinoma
Colorectal Neoplasms - genetics
Colorectal Neoplasms - pathology
CpG islands
CpG Islands - genetics
Datasets as Topic
Deoxyribonucleic acid
DNA
DNA (Cytosine-5-)-Methyltransferases - genetics
DNA (Cytosine-5-)-Methyltransferases - metabolism
DNA Methylation
DNA methyltransferase
Elongation
Epigenesis, Genetic
Gene Expression Regulation, Neoplastic
Gene Knockout Techniques
Histone Code - genetics
Histones
Histones - genetics
Humanities and Social Sciences
Humans
Islands
MLH1 protein
multidisciplinary
Nucleotide sequence
Promoter Regions, Genetic - genetics
Science
Science (multidisciplinary)
Suppressors
Transcription elongation
Transcription, Genetic
Tumorigenesis
Tumors
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Title De novo DNA methyltransferase activity in colorectal cancer is directed towards H3K36me3 marked CpG islands
URI https://link.springer.com/article/10.1038/s41467-020-20716-w
https://www.ncbi.nlm.nih.gov/pubmed/33514701
https://www.proquest.com/docview/2483414217
https://www.proquest.com/docview/2483811737
https://pubmed.ncbi.nlm.nih.gov/PMC7846778
https://doaj.org/article/9803ec9958634a5e94312be4787e0b29
Volume 12
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