The nonviral episomal replicating vector pEPI-1 allows long-term inhibition of bcr-abl expression by shRNA

Hum Gene Ther. 2005 Apr;16(4):533-9. doi: 10.1089/hum.2005.16.533.

Abstract

The inhibition of gene expression by RNA interference harbors a high potential for application in the therapy of human diseases. However, while exogenous application of siRNAs efficiently inhibits gene expression, these effects are only transient in mammalian cells. We designed a short hairpin RNA-expression cassette to target the bcr-abl oncogene that was then introduced into the nonviral vector system pEPI-1, which replicates episomally in the absence of selection in the bcr-abl-positive cell line K562. Forty-two days after transfection the bcr-abl- but not the cytokine-dependent growth rate was found to be drastically reduced in K562 cells. Western analysis revealed a more than 90% reduction in the expression of the fusion protein bcr-abl while the expression of the bcr protein remained unaffected. In addition, we show that the level of bcr-abl mRNA was specifically reduced in these cells for more than 90%. These results demonstrate that the vector system pEPI-1 allows specific and efficient long term gene suppression by using a short hairpin RNA transcription unit.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Base Sequence
  • Blotting, Northern
  • Blotting, Western
  • Cell Proliferation
  • Cytokines / metabolism
  • DNA Polymerase III / genetics
  • Fusion Proteins, bcr-abl / drug effects
  • Fusion Proteins, bcr-abl / genetics*
  • Gene Expression Regulation / drug effects
  • Genetic Vectors / genetics*
  • Genetic Vectors / pharmacology
  • Humans
  • K562 Cells
  • Molecular Sequence Data
  • Plasmids / genetics*
  • Promoter Regions, Genetic
  • RNA / chemistry
  • RNA / genetics
  • RNA / pharmacology*
  • RNA, Catalytic / chemistry
  • Virus Replication / genetics*

Substances

  • Cytokines
  • RNA, Catalytic
  • hairpin ribozyme
  • RNA
  • Fusion Proteins, bcr-abl
  • DNA Polymerase III