CpG methylation is maintained in human cancer cells lacking DNMT1 View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2000-04

AUTHORS

Ina Rhee, Kam-Wing Jair, Ray-Whay Chiu Yen, Christoph Lengauer, James G. Herman, Kenneth W. Kinzler, Bert Vogelstein, Stephen B. Baylin, Kornel E. Schuebel

ABSTRACT

Hypermethylation is associated with the silencing of tumour susceptibility genes in several forms of cancer; however, the mechanisms responsible for this aberrant methylation are poorly understood. The prototypic DNA methyltransferase, DNMT1, has been widely assumed to be responsible for most of the methylation of the human genome, including the abnormal methylation found in cancers. To test this hypothesis, we disrupted the DNMT1 gene through homologous recombination in human colorectal carcinoma cells. Here we show that cells lacking DNMT1 exhibited markedly decreased cellular DNA methyltransferase activity, but there was only a 20% decrease in overall genomic methylation. Although juxtacentromeric satellites became significantly demethylated, most of the loci that we analysed, including the tumour suppressor gene p16INK4a, remained fully methylated and silenced. These results indicate that DNMT1 has an unsuspected degree of regional specificity in human cells and that methylating activities other than DNMT1 can maintain the methylation of most of the genome. More... »

PAGES

1003

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/35010000

DOI

http://dx.doi.org/10.1038/35010000

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1001213938

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/10801130


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