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Histone deacetylase 11 suppresses p53 expression in pituitary tumor cells

Weimin Wang1,2, Li Fu2, Shengli Li2

  • 1School of Medicine, Shandong University, Jinan, 250012, China.

Cell Biology International
|August 8, 2017
PubMed

Insights

Histone deacetylase 11 (HDAC11) interferes with p53 expression in pituitary tumors (PT), promoting tumor growth. Inhibiting HDAC11 may offer a new therapeutic strategy for treating PT.

Area of Science:

  • Endocrinology
  • Molecular Biology
  • Oncology

Background:

  • The precise mechanisms driving pituitary tumor (PT) pathogenesis remain elusive.
  • Disrupted apoptosis is a key contributor to tumor progression.
  • Histone deacetylases (HDAC) are critical regulators of cellular processes, including apoptosis.

Purpose of the Study:

  • To investigate the role of HDACs in modulating apoptosis within pituitary tumors.
  • To explore the specific involvement of HDAC11 in PT development and its relationship with p53.

Main Methods:

  • Analysis of HDAC and p53 expression in 20 human PT samples.
  • In vitro studies using the AtT-20 pituitary tumor cell line to assess HDAC's impact on apoptosis.
  • Detection of protein complexes and analysis of gene transcription activity at the p53 promoter locus.

Main Results:

  • Elevated HDAC11 and reduced p53 levels were observed in PT samples, showing a negative correlation.
  • HDAC11 formed a complex with HEY1, a p53 transcription factor, leading to decreased HEY1 acetylation and transcriptional activity at the p53 promoter.
  • Overexpression of HDAC11 mimicked these effects in AtT-20 cells, while HDAC11 knockdown restored p53 expression.

Conclusions:

  • HDAC11 directly interferes with p53 expression in pituitary tumor cells.
  • Targeting HDAC11 presents a promising therapeutic avenue for pituitary tumor treatment.
Keywords:
apoptosishistone deacetylasep53pituitary tumor

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