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Loss of Tumor Suppressor Gene Functions

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...

Loss of Tumor Suppressor Gene Functions

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 Genes

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...

Cancer-Critical Genes II: Tumor Suppressor Genes

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...

Abnormal Proliferation

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...

The Retinoblastoma Gene

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...

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Related Experiment Video

Updated: Jun 16, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

A tumor suppressor SIRTainty.

Paul T Schumacker¹

¹Department of Pediatrics, Robert F Lurie Comprehensive Cancer Center, Northwestern University Feinberg School of Medicine, Chicago, IL 60611, USA. p-schumacker@northwestern.edu

|February 5, 2010

Summary

This summary is machine-generated.

SIRT3 acts as a tumor suppressor by boosting mitochondrial MnSOD, crucial for longevity and stress response. Its loss promotes cancer growth via increased reactive oxygen species (ROS).

Related Experiment Videos

Last Updated: Jun 16, 2026

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates

Published on: February 27, 2016

Area of Science:

Molecular Biology
Oncology
Biochemistry

Background:

Sirtuin deacetylases (SIRTs) are NAD+-dependent enzymes involved in cellular metabolism, aging, and stress resistance.
SIRT3, a mitochondrial sirtuin, plays a critical role in regulating mitochondrial function and cellular homeostasis.
Dysregulation of sirtuins, including SIRT3, has been implicated in various diseases, including cancer.

Discussion:

Kim et al. demonstrate that SIRT3 functions as a tumor suppressor in cancer.
SIRT3 enhances the expression of mitochondrial manganese superoxide dismutase (MnSOD), a key antioxidant enzyme.
Loss of SIRT3 function leads to elevated levels of mitochondrial reactive oxygen species (ROS).

Key Insights:

SIRT3-mediated upregulation of MnSOD is essential for mitigating oxidative stress within mitochondria.
Increased mitochondrial ROS due to SIRT3 deficiency promotes cellular transformation and tumor progression.
These findings highlight SIRT3 as a potential therapeutic target for cancer treatment.

Outlook:

Further research is warranted to explore the precise mechanisms by which SIRT3 regulates MnSOD expression.
Investigating the therapeutic potential of targeting SIRT3 in various cancer types could lead to novel treatment strategies.
Understanding the interplay between SIRT3, mitochondrial ROS, and cancer development may offer new avenues for cancer prevention and therapy.