Histone deacetylase inhibitor-induced cellular apoptosis involves stanniocalcin-1 activation

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Assays for Validating Histone Acetyltransferase Inhibitors
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Published on: August 6, 2020

A Y S Law1, K P Lai, W C Lui

  • 1Department of Biology, Hong Kong Baptist University, Kowloon Tong, Hong Kong.

Experimental Cell Research
|July 26, 2008
PubMed

Insights

Histone deacetylase inhibitor trichostatin A (TSA) induces stanniocalcin-1 (STC1) expression and apoptosis in cancer cells. This occurs via histone hyper-acetylation and NF-kappaB activation, with STC1 promoting apoptosis.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Epigenetics

Background:

  • Previous studies implicated HIF-1 and p53 in stanniocalcin-1 (STC1) gene transcription regulation in human cancer cells.
  • Histone deacetylase (HDAC) inhibitors are known to affect cellular processes, including apoptosis and gene expression.

Purpose of the Study:

  • To investigate the effect of HDAC inhibition on STC1 expression and apoptosis in human cancer cells.
  • To elucidate the molecular mechanisms underlying TSA-induced STC1 gene expression and its role in apoptosis.

Main Methods:

  • Treatment of human colon adenoma HT29 cells and other cancer cell lines (SKOV3, CaCo-2, Jurkat, CNE-2) with trichostatin A (TSA).
  • Analysis of STC1 mRNA and protein levels, cellular apoptosis, histone acetylation, and NF-kappaB activation.
  • Chromatin immunoprecipitation (ChIP) assays, reporter gene assays, and gene silencing experiments.

Main Results:

  • TSA treatment induced cellular apoptosis and STC1 expression across multiple human cancer cell lines.
  • STC1 induction was rapid, transcriptionally regulated, and correlated with increased histone H3/H4 acetylation and NF-kappaB activation.
  • NF-kappaB activation was crucial for TSA-induced STC1 expression, and STC1 silencing reduced TSA-induced apoptosis.

Conclusions:

  • Histone hyper-acetylation and NF-kappaB recruitment stimulate STC1 gene expression in response to HDAC inhibition.
  • STC1 acts as a pro-apoptotic factor, mediating the apoptotic effects of TSA in cancer cells.
  • This study reveals a novel epigenetic mechanism regulating STC1 and highlights its role in cancer cell death.

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