Role of class I and class II histone deacetylases in carcinoma cells using siRNA

Biochem Biophys Res Commun. 2003 Oct 17;310(2):529-36. doi: 10.1016/j.bbrc.2003.09.043.

Abstract

The role of the individual histone deacetylases (HDACs) in the regulation of cancer cell proliferation was investigated using siRNA-mediated protein knockdown. The siRNA for HDAC3 and HDAC1 demonstrated significant morphological changes in HeLa S3 consistent with those observed with HDAC inhibitors. SiRNA for HDAC 4 or 7 produced no morphological changes in HeLa S3 cells. HDAC1 and 3 siRNA produced a concentration-dependent inhibition of HeLa cell proliferation; whereas, HDAC4 and 7 siRNA showed no effect. HDAC3 siRNA caused histone hyperacetylation and increased the percent of apoptotic cells. These results demonstrate that the Class I HDACs such as HDACs 1 and 3 are important in the regulation of proliferation and survival in cancer cells. These results and the positive preclinical results with non-specific inhibitors of the HDAC enzymes provide further support for the development of Class I selective HDAC inhibitors as cancer therapeutics.

MeSH terms

  • Acetylation
  • Antineoplastic Agents / pharmacology
  • Apoptosis
  • Carcinoma / enzymology*
  • Carcinoma / genetics
  • Carcinoma / pathology
  • Cell Division / drug effects
  • HeLa Cells
  • Histone Deacetylases / classification
  • Histone Deacetylases / genetics
  • Histone Deacetylases / physiology*
  • Histones / metabolism
  • Humans
  • RNA Interference
  • RNA, Small Interfering / pharmacology

Substances

  • Antineoplastic Agents
  • Histones
  • RNA, Small Interfering
  • Histone Deacetylases