[Effect of curcumin on acetylation of histone H3 in human lymphoma cell line Raji]

Ai Zheng. 2006 May;25(5):582-6.
[Article in Chinese]

Abstract

Background & objective: Epigenetic change is an important mechanism of oncogenesis. The inhibitors of methyltransferases and deacetylases, with epigenetic modificative effects, could inhibit proliferation and induce apoptosis of tumor cells. This study was to investigate the effects of curcumin on the acetylation of histone H3 and the expression of p21(WAF1/CIP1) gene in human lymphoma cell line Raji.

Methods: Raji cells were treated with 25 micromol/L curcumin. The levels of acetylated histone H3 and p21WAF1/CIP1 were detected by Western blot, the expression of p21(WAF1/CIP1) gene was detected by reverse transcription-polymerase chain reaction (RT-PCR), and the level of acetylated histone H3 at the site of p21(WAF1/CIP1) promoter gene was examined by chromatin immunoprecipitation assay. Cell cycle distribution was studied by flow cytometry.

Results: Curcumin induced hyperacetylation of histone H3 at the site of p21(WAF1/CIP1) promoter by 1.9 folds, and enhanced the levels of p21(WAF1/CIP1) mRNA by 4.2 folds and protein by 5.1 folds 24 h after treatment. Raji cells were arrested at G(2)/M phase when treated with curcumin for 24 h, and at G(0)/G(1) phase when treated for 36 h.

Conclusion: Curcumin, with epigenetic modificative effects, could enhance the acetylayion of histone H3 at the site of p21(WAF1/CIP1) promoter gene, improve transcription of p21(WAF1/CIP1) gene, and arrest cell cycle progression of Raji cells.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acetylation / drug effects
  • Antineoplastic Agents / pharmacology
  • Cell Cycle / drug effects
  • Cell Line, Tumor
  • Curcumin / pharmacology*
  • Cyclin-Dependent Kinase Inhibitor p21 / biosynthesis*
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics
  • Epigenesis, Genetic
  • Histones / genetics
  • Histones / metabolism*
  • Humans
  • Lymphoma, B-Cell / metabolism*
  • Lymphoma, B-Cell / pathology
  • Promoter Regions, Genetic
  • RNA, Messenger / metabolism

Substances

  • Antineoplastic Agents
  • CDKN1A protein, human
  • Cyclin-Dependent Kinase Inhibitor p21
  • Histones
  • RNA, Messenger
  • Curcumin