Deficiency of Mbd2 suppresses intestinal tumorigenesis

Nat Genet. 2003 Jun;34(2):145-7. doi: 10.1038/ng1155.

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