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Updated: Feb 9, 2026

An Engineered Split-TET2 Enzyme for Chemical-inducible DNA Hydroxymethylation and Epigenetic Remodeling
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Epigenetic dysregulation of TET2 in human glioblastoma

María G García1,2, Antonella Carella1,2, Rocío G Urdinguio2

  • 1Institute of Oncology of Asturias (IUOPA), HUCA, Universidad de Oviedo, Oviedo, Spain.

Oncotarget
|June 15, 2018
PubMed

Insights

Epigenetic alterations in Ten-eleven translocation 2 (TET2) are common in glioblastoma. Restoring TET2 function in glioblastoma cells reduced tumor growth and promoted neural differentiation.

Area of Science:

  • Oncology
  • Epigenetics
  • Molecular Biology

Background:

  • Ten-eleven translocation (TET) enzymes are crucial for DNA demethylation and epigenetic regulation.
  • TET enzyme deregulation is implicated in various cancers, but mechanisms in glioblastoma remain unclear.

Purpose of the Study:

  • To investigate the role of TET2 epigenetic alterations in human glioblastoma.
  • To explore the functional impact of TET2 restoration on glioblastoma cell behavior.

Main Methods:

  • Analysis of epigenetic modifications (DNA methylation, hydroxymethylation, histone acetylation) in TET2 in glioblastoma samples.
  • Ectopic expression of TET2 in glioblastoma cell lines.
  • Assessment of neural differentiation and tumor growth in vitro and in vivo.

Main Results:

  • Frequent epigenetic alterations of TET2, including DNA hypermethylation and hypo-hydroxymethylation, were observed in glioblastoma.
  • Loss of histone acetylation at TET2 was also noted.
  • Ectopic TET2 overexpression induced neural differentiation and inhibited glioblastoma cell growth.

Conclusions:

  • Epigenetic dysregulation of TET2 is a significant factor in human glioblastoma development.
  • Targeting TET2 may offer a therapeutic strategy for glioblastoma.
Keywords:
5-hydroxymehtylcytosineDNA methylationTET2epigeneticsglioblastoma

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