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Tumors smother their epigenome.

Bernard Thienpont1, Laurien Van Dyck1, Diether Lambrechts1

  • 1Vesalius Research Center, VIB, Leuven, Belgium; Laboratory of Translational Genetics, Department of Oncology, KU Leuven, Leuven, Belgium.

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Summary

Hypoxia in tumors compromises DNA demethylation enzymes, leading to DNA hypermethylation. This epigenetic change inactivates genes, linking the tumor microenvironment to cancer progression.

Keywords:
5-hydroxymethylcytosine5-methylcytosineDNA hypermethylationHypoxiaTET1TET2TET3oncogenesis

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Area of Science:

  • Epigenetics
  • Cancer Biology
  • Tumor Microenvironment

Background:

  • DNA hypermethylation is a common event in cancer.
  • The triggers for DNA hypermethylation in tumors remain largely unidentified.
  • The tumor microenvironment, particularly hypoxia, may influence epigenetic modifications.

Purpose of the Study:

  • To investigate the role of hypoxia in DNA hypermethylation within tumors.
  • To explore the impact of compromised DNA demethylation on gene expression in cancer cells.

Main Methods:

  • Assessing the activity of 10-11-translocation methylcytosine dioxygenases in hypoxic tumor models.
  • Analyzing gene methylation patterns and expression levels in relation to tumor hypoxia.

Main Results:

  • The activity of 10-11-translocation methylcytosine dioxygenases is reduced under hypoxic conditions.
  • Compromised DNA demethylation leads to an accumulation of DNA hypermethylation in tumors.
  • This hypermethylation results in the inactivation of critical genes associated with cancer.

Conclusions:

  • Hypoxia in the tumor microenvironment directly contributes to DNA hypermethylation.
  • The inactivation of DNA demethylation pathways by hypoxia represents a key mechanism linking the tumor microenvironment to cancer-associated epigenetic alterations.