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Decrease of 5-hydroxymethylcytosine in rat liver with subchronic exposure to genotoxic carcinogens riddelliine and
Christine Guo Lian1, Shuyun Xu1, Weimin Guo1
1Program in Dermatopathology, Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.
Molecular Carcinogenesis
|August 27, 2014
Summary
Levels of 5-hydroxymethylcytosine (5-hmC) and TET2 expression decreased in rat livers exposed to genotoxic carcinogens. This epigenetic alteration suggests a role for TET2-mediated 5-hydroxymethylation in early carcinogenesis.
Area of Science:
- Epigenetics
- Cancer Biology
- Toxicology
Background:
- 5-hydroxymethylcytosine (5-hmC) levels are reduced in established cancers.
- The role of 5-hmC in the early stages of carcinogenesis induced by genotoxic agents remains unclear.
Purpose of the Study:
- To investigate the impact of genotoxic carcinogens on 5-hmC levels and TET2 expression in early carcinogenesis.
- To determine if alterations in 5-hmC are associated with carcinogen-induced genetic mutations.
Main Methods:
- Rats were treated with genotoxic carcinogens (riddelliine or aristolochic acid).
- Liver tissues were analyzed for 5-hmC levels and TET2 expression.
Main Results:
- Both 5-hmC levels and TET2 expression were significantly decreased in the livers of carcinogen-treated rats.
- The observed loss of 5-hmC correlated with the induction of genetic mutations by the carcinogens.
Conclusions:
- Genotoxic carcinogens disrupt TET2-mediated 5-hydroxymethylation in the early stages of carcinogenesis.
- Epigenetic modifications, specifically the loss of 5-hmC, may play a crucial role in the initial development of cancer.
