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Epigenetic Regulation

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...

Epigenetic Regulation

Epigenetic Regulation

Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.

Background and Environment Affect Phenotype

Background and Environment Affect Phenotype

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Mutagenicity and Carcinogenicity

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...

Inheritance of Chromatin Structures

Inheritance of Chromatin Structures

Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying DNA...

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The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...

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Related Experiment Video

Updated: Jun 4, 2026

In Vitro Scratch Assay to Demonstrate Effects of Arsenic on Skin Cell Migration

In Vitro Scratch Assay to Demonstrate Effects of Arsenic on Skin Cell Migration

Published on: February 23, 2019

Epigenetic changes in individuals with arsenicosis.

Lisa Smeester¹, Julia E Rager, Kathryn A Bailey

¹Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, UNC-Chapel Hill, Chapel Hill, North Carolina 27599, United States.

Chemical Research in Toxicology

|February 5, 2011

Summary

Millions worldwide suffer from inorganic arsenic (iAs) poisoning. This study reveals iAs silences tumor suppressor genes, offering a key insight into arsenic-induced diseases like cancer via epigenetic changes.

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Area of Science:

Environmental Health
Epigenetics
Toxicology

Background:

Inorganic arsenic (iAs) is a widespread environmental toxicant.
Chronic exposure leads to arsenicosis and arsenic poisoning.
Arsenic exposure is linked to various chronic diseases.

Purpose of the Study:

To investigate the epigenetic mechanisms underlying arsenic-induced diseases.
To identify gene methylation changes associated with chronic arsenic exposure.
To uncover specific gene complexes affected by arsenic toxicity.

Main Methods:

Utilized advanced methylome mapping techniques.
Analyzed gene methylation patterns in study subjects exposed to arsenic.
Identified a network of hypermethylated genes.

Main Results:

Discovered a large interactome of hypermethylated genes.
These genes are significantly enriched in pathways related to cancer, heart disease, and diabetes.
Identified a novel 'arsenic-induced tumor suppressorome' of 17 silenced tumor suppressor genes.

Conclusions:

Arsenic exposure induces widespread epigenetic alterations.
Silencing of tumor suppressor genes by arsenic represents a potential epigenetic mechanism for arsenic-induced carcinogenesis.
Findings provide critical insights into the pathogenesis of arsenic-associated diseases.