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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.

Molecular & Cellular Oncology
|January 17, 2017
PubMed

Insights

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

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.
Keywords:
5-hydroxymethylcytosine5-methylcytosineDNA hypermethylationHypoxiaTET1TET2TET3oncogenesis

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