Related Experiment Video

Updated: Aug 26, 2026

Assays for Validating Histone Acetyltransferase Inhibitors
09:11

Assays for Validating Histone Acetyltransferase Inhibitors

Published on: August 6, 2020

[Histone deacetylase inhibitor blocks proliferation of cells transformed with oncogenes E1A and cHa-ras]

M V Abramova1, S B Svetlikova, N D Aksenov

  • 1Institute of Cytology RAS, St. Petersburg. mav@mail.cytspb.rssi.ru

Tsitologiia
|March 3, 2004
PubMed

Insights

Sodium butyrate restores cell cycle control in cancer cells by inhibiting histone deacetylase activity. This treatment reactivates tumor suppressor proteins, offering a potential therapeutic strategy for cancer.

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Context:

  • Transformed rat embryonic fibroblasts with E1A and cHa-ras oncogenes exhibit cell cycle dysregulation.
  • These cells fail to arrest at checkpoints under conditions of growth factor deprivation and genotoxic stress.

Purpose:

  • To investigate the effect of sodium butyrate (NaB), a histone deacetylase inhibitor, on cell cycle progression in oncogene-transformed fibroblasts.
  • To elucidate the molecular mechanisms underlying NaB's impact on cell cycle regulators.

Summary:

  • Sodium butyrate treatment induced G1/S and G2/M cell cycle blocks in transformed fibroblasts.
  • NaB altered the expression of cyclins (D1, A, E) and cyclin-dependent kinases (Cdk2, Cdk4), while increasing the levels of p21Waf1 and p27Kip1 inhibitors.
  • The study suggests NaB restores the inhibitory function of p21Waf1 by promoting its binding to Cdk2, potentially through the activation of novel HDAC-dependent genes.

Impact:

  • Sodium butyrate treatment can restore cell cycle checkpoint control in cancer cells.
  • This highlights the potential of histone deacetylase inhibitors as therapeutic agents in oncology.
  • The findings provide insights into the interplay between oncogene expression, epigenetic modifications, and cell cycle regulation.

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