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Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers
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Repressing Gene Transcription by Redirecting Cellular Machinery with Chemical Epigenetic Modifiers

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HDAC1-mSin3a-NCOR1, Dnmt3b-HDAC1-Egr1 and Dnmt1-PCNA-UHRF1-G9a regulate the NY-ESO1 gene expression

Pierre-François Cartron1, Christophe Blanquart, Eric Hervouet

  • 1Centre de Recherche en Cancérologie Nantes-Angers, INSERM U892, Equipe Apoptose et Progression Tumorale, Equipe labellisée Ligue Nationale Contre le Cancer, 8 Quai Moncousu, BP 7021, 44007 Nantes, France. pierre-francois.cartron@univ-nantes.fr

Molecular Oncology
|January 15, 2013
PubMed

Insights

The NY-ESO1 gene, a cancer/testis antigen, is epigenetically silenced in tumors. This study reveals a sequential mechanism involving histone deacetylation, methylation, and DNA methylation in glioma and mesothelioma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Epigenetics

Background:

  • The NY-ESO1 gene is a cancer/testis antigen and a potential target for cancer immunotherapy.
  • Epigenetic silencing of the NY-ESO1 gene is observed in various tumors, but the underlying molecular mechanisms remain unclear.

Purpose of the Study:

  • To elucidate the molecular mechanisms of epigenetic regulation and silencing of the NY-ESO1 gene in non-epithelial cancers.
  • To investigate the sequential recruitment of epigenetic modifiers involved in NY-ESO1 gene silencing.

Main Methods:

  • Analysis of epigenetic regulation in glioma and mesothelioma cell lines.
  • Identification of protein complexes involved in histone deacetylation, histone methylation, and DNA methylation.

Main Results:

  • The epigenetic regulation of the NY-ESO1 gene involves the sequential recruitment of specific protein complexes.
  • Key complexes identified include HDAC1-mSin3a-NCOR, Dnmt3b-HDAC1-Egr1, and Dnmt1-PCNA-UHRF1-G9a.
  • This orchestration involves coordinated histone deacetylation, histone methylation, and DNA methylation processes.

Conclusions:

  • The study demonstrates a sequential epigenetic mechanism responsible for NY-ESO1 gene silencing in glioma and mesothelioma.
  • Understanding this mechanism provides insights into cancer/testis antigen regulation and potential therapeutic strategies for malignancies.

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