Abstract
Gene silencing through de novo methylation of CpG island promoters contributes to cancer. We find that Mbd2, which recruits co-repressor complexes to methylated DNA, is essential for efficient tumorigenesis in the mouse intestine. As Mbd2-deficient mice are viable and fertile, their resistance to intestinal cancer may be of therapeutic relevance.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adenoma / etiology
-
Adenoma / genetics
-
Adenoma / pathology
-
Adenoma / prevention & control
-
Animals
-
CpG Islands
-
DNA Methylation
-
DNA-Binding Proteins / deficiency*
-
DNA-Binding Proteins / genetics
-
Gene Silencing
-
Genes, APC
-
Heterozygote
-
Homozygote
-
Intestinal Neoplasms / etiology
-
Intestinal Neoplasms / genetics
-
Intestinal Neoplasms / pathology
-
Intestinal Neoplasms / prevention & control*
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
Substances
-
DNA-Binding Proteins
-
MBD2 protein