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PMID: 15156141 Published · ppublish English Journal Article

CpG island hypermethylation is maintained in human colorectal cancer cells after RNAi-mediated depletion of DNMT1.

Nature genetics ·Vol. 36 ·No. 6 ·2004-06-00 ·Pages 582-4

Ting AH, Jair KW, Suzuki H, Yen RW, Baylin SB, Schuebel KE

Abstract

The role of the primary mammalian DNA methyltransferase, DNMT1, in maintaining CpG island methylation in human colon cancer cells has recently been questioned. This controversy has arisen from discrepancies between genetic knockout and RNA interference-mediated knockdown studies. Here, we re-examined the RNA interference-based approach and found that hypermethylation of single-copy genes is maintained in cells transiently and stably depleted of DNMT1.

MeSH Terms
Base Sequence Colorectal Neoplasms/enzymology,genetics CpG Islands DNA (Cytosine-5-)-Methyltransferase 1 DNA (Cytosine-5-)-Methyltransferases/antagonists & inhibitors,genetics,metabolism DNA Methylation Gene Silencing Genes, Tumor Suppressor HCT116 Cells Humans Promoter Regions, Genetic RNA Interference RNA, Neoplasm/genetics RNA, Small Interfering/genetics
Chemicals
RNA, Neoplasm RNA, Small Interfering DNA (Cytosine-5-)-Methyltransferase 1 DNA (Cytosine-5-)-Methyltransferases DNMT1 protein, human
Authors & Affiliations
6 authors, click to expand affiliations / ORCID
Ting Angela H
Program in Cellular and Molecular Medicine, Cancer Biology Division, The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins, The Johns Hopkins University, Baltimore, Maryland 21231, USA.
Jair Kam-wing
Suzuki Hiromu
Yen Ray-Whay Chiu
Baylin Stephen B
Schuebel Kornel E
Article Info
Journal
Nature genetics
Abbr.
Nat Genet
ISSN
1061-4036
Published
2004-06-00
Epub
2004-00-23
Pages
582-4
Language
English
Region
United States
NLM ID
9216904
Subset
IM
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