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Histone deacetylase inhibitor scriptaid induces cell cycle arrest and epigenetic change in colon cancer cells

Eun Ju Lee1, Bo Bin Lee, Soon-Ja Kim

  • 1Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 440-746, Korea.

International Journal of Oncology
|September 25, 2008
PubMed

Insights

Scriptaid, a histone deacetylase inhibitor (HDACI), suppresses colorectal cancer cell growth and induces cell cycle arrest. It also reverses epigenetic silencing of the p16 gene by reducing repressive chromatin marks.

Area of Science:

  • Epigenetics
  • Cancer Biology
  • Molecular Pharmacology

Background:

  • Histone deacetylase inhibitors (HDACIs) regulate crucial cellular processes like growth, apoptosis, and differentiation.
  • Aberrant epigenetic modifications, including DNA methylation and histone alterations, are implicated in colorectal cancer pathogenesis.
  • The p16 gene is frequently silenced in cancer via promoter hypermethylation, leading to uncontrolled cell proliferation.

Purpose of the Study:

  • To investigate the effects of the HDACI scriptaid on histone modification, gene demethylation, cell cycle progression, and apoptosis in RKO colorectal cancer cells.
  • To identify genes modulated by scriptaid treatment in colorectal cancer.
  • To explore the synergistic potential of scriptaid with 5-aza-2'-deoxycytidine (5-aza-dC) in reversing epigenetic silencing.

Main Methods:

  • RKO cells were treated with scriptaid, 5-aza-dC, or trichostatin A (TSA).
  • Chromatin immunoprecipitation and methylation-specific PCR were used to analyze histone modifications and p16 gene methylation.
  • Flow cytometry assessed cell cycle distribution and apoptosis, while gene expression profiling identified scriptaid-induced genes.

Main Results:

  • Scriptaid induced demethylation and re-expression of the hypermethylated p16 gene, synergistically with 5-aza-dC.
  • Scriptaid modulated histone modifications, increasing euchromatic marks (acetyl-H3-K9, dimethyl-H3-K4) and decreasing a repressive mark (dimethyl-H3-K9).
  • Scriptaid inhibited RKO cell growth dose-dependently, induced G1 and G2/M cell cycle arrest, and altered expression of 278 genes, without significantly affecting apoptosis.

Conclusions:

  • Scriptaid demonstrates potential for colorectal cancer therapy through growth suppression and cell cycle arrest.
  • Scriptaid can reverse repressive chromatin marks at the p16 promoter, restoring gene expression.
  • The findings suggest scriptaid's efficacy in targeting epigenetic dysregulation in colorectal cancer.

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