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Histone deacetylase 2 controls p53 and is a critical factor in tumorigenesis

Tobias Wagner1, Peter Brand1, Thorsten Heinzel1

  • 1Center for Molecular Biomedicine, Institute of Biochemistry and Biophysics, Department of Biochemistry, Friedrich Schiller University of Jena, Hans-Knöll-Str. 2, 07745 Jena, Germany.

Biochimica Et Biophysica Acta
|July 30, 2014
PubMed

Insights

Histone deacetylase 2 (HDAC2) is overexpressed in cancers and impacts the tumor suppressor p53. Understanding their interaction is key for developing new cancer therapies.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • Histone deacetylase 2 (HDAC2) regulates cellular processes via protein deacetylation.
  • HDAC2 overexpression is common in various cancers, implicating it in cancer progression.
  • TP53 gene mutations and p53 inactivation are frequent in human tumors, with incompletely understood mechanisms.

Purpose of the Study:

  • To summarize recent findings on HDAC2 overexpression in cancer.
  • To elucidate the mechanisms connecting HDAC2 and the tumor suppressor p53.
  • To present a model of the interplay between p53 and HDAC2.

Main Methods:

  • Literature review of in vitro and in vivo studies.
  • Analysis of molecular pathways regulating HDAC2 and p53.
  • Integration of feedback loops involving transcription factors.

Main Results:

  • HDAC2 is linked to p53 regulation through deacetylation and maintenance of genomic stability.
  • HDAC2 overexpression is observed in both solid and hematopoietic malignancies.
  • A model is presented detailing how p53 and other factors regulate HDAC2 and p53 expression and degradation.

Conclusions:

  • The interaction between p53 and HDAC2 is crucial in cancer biology.
  • Understanding these molecular mechanisms can inform novel therapeutic strategies.
  • Targeting the HDAC2-p53 axis may offer new avenues for cancer treatment.
Keywords:
CancerHDAC inhibitorsHDAC2RLIMSumoylationp53

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