Related Experiment Video

Updated: Aug 8, 2026

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 29, 2010

Deficiency of Mbd2 suppresses intestinal tumorigenesis

Owen J Sansom1, Jennifer Berger, Stefan M Bishop

  • 1Cardiff School of Biosciences, Cardiff University, Cardiff, Wales, UK.

Nature Genetics
|May 6, 2003
PubMed

Insights

Methyl-CpG-binding domain protein 2 (Mbd2) is crucial for intestinal cancer development in mice. Mbd2 deficiency prevents tumor growth, suggesting therapeutic potential for targeting Mbd2 in cancer treatment.

Area of Science:

  • Epigenetics and Cancer Biology
  • Molecular Oncology
  • Gene Regulation

Background:

  • Gene silencing via DNA methylation of CpG islands is a known mechanism in cancer development.
  • Methyl-CpG-binding domain protein 2 (Mbd2) plays a role in recruiting co-repressor complexes to methylated DNA.

Purpose of the Study:

  • To investigate the role of Mbd2 in intestinal tumorigenesis.
  • To determine the therapeutic relevance of Mbd2 deficiency in a mouse model of intestinal cancer.

Main Methods:

  • Utilized a mouse model to study intestinal cancer development.
  • Assessed the impact of Mbd2 deficiency on tumorigenesis.
  • Observed the physiological state of Mbd2-deficient mice.

Main Results:

  • Mbd2 was found to be essential for efficient intestinal tumor formation in mice.
  • Mice lacking Mbd2 were resistant to intestinal cancer development.
  • Mbd2-deficient mice exhibited normal viability and fertility.

Conclusions:

  • Mbd2 is a critical mediator of de novo methylation-driven gene silencing in intestinal cancer.
  • The absence of Mbd2 confers resistance to intestinal tumorigenesis.
  • Targeting Mbd2 presents a potential therapeutic strategy for intestinal cancer.

More Related Videos

A Simple Device to Rapidly Prepare Whole Mounts of the Mouse Intestine05:49

A Simple Device to Rapidly Prepare Whole Mounts of the Mouse Intestine

Published on: October 27, 2015

3D Culturing of Organoids from the Intestinal Villi Epithelium Undergoing Dedifferentiation06:40

3D Culturing of Organoids from the Intestinal Villi Epithelium Undergoing Dedifferentiation

Published on: April 1, 2021

Related Concept Videos

Mismatch Repair01:36

Mismatch Repair

Overview
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...