Related Experiment Video

Updated: Aug 16, 2026

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
10:41

An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues

Published on: April 5, 2018

The sno gene, which encodes a component of the histone deacetylase complex, acts as a tumor suppressor in mice

T Shinagawa1, H D Dong, M Xu

  • 1Laboratory of Molecular Genetics, RIKEN Tsukuba Life Sciences Center, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japa.

The EMBO Journal
|May 16, 2000
PubMed

Insights

Loss of the Sno oncoprotein increases cancer susceptibility in mice. Sno acts as a tumor suppressor, as heterozygous mice show increased tumor formation and resistance to apoptosis.

Area of Science:

  • Molecular Biology
  • Oncology
  • Developmental Biology

Background:

  • Ski and Sno oncoproteins are part of a complex involved in transcriptional repression.
  • This complex negatively regulates transforming growth factor-beta (TGF-beta) signaling by interacting with Smads.

Purpose of the Study:

  • To investigate the role of Sno in tumorigenesis and embryonic development.
  • To determine if Sno functions as a tumor suppressor.

Main Methods:

  • Analysis of sno heterozygous mice (sno(+/-)) for tumor development and embryonic lethality.
  • Assessment of embryonic fibroblasts from sno(+/-) mice for proliferative capacity and transformation.
  • Evaluation of apoptosis and cell cycle arrest sensitivity in B cells, T cells, and embryonic fibroblasts from sno(+/-) mice.

Main Results:

  • Mice lacking sno died during embryogenesis, indicating its essential role in development.
  • sno(+/-) mice exhibited increased susceptibility to spontaneous and chemically induced tumors.
  • sno(+/-) cells showed increased proliferation, neoplastic transformation potential, and resistance to apoptosis and cell cycle arrest.

Conclusions:

  • Sno functions as a tumor suppressor, at least in certain cell types.
  • Loss of Sno function compromises cellular mechanisms that prevent uncontrolled growth and promote cell death, leading to increased cancer risk.

More Related Videos

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers10:28

Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

Published on: September 20, 2018

Assays for Validating Histone Acetyltransferase Inhibitors09:11

Assays for Validating Histone Acetyltransferase Inhibitors

Published on: August 6, 2020

Related Concept Videos

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...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Epigenetic Regulation01:37

Epigenetic Regulation

Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
X-chromosome...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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...