A homologous promoterless K-ras cDNA targeting endogenous K-ras expression inhibits human pancreatic cancer cell growth in vitro and in vivo

Cancer Biol Ther. 2008 Oct;7(10):1641-7. doi: 10.4161/cbt.7.10.6586. Epub 2008 Oct 9.

Abstract

It has been reported that the local introduction of a promoter-less DNA containing the complementary DNA (cDNA) sequence of a gene could induce gene-specific silencing in plants. The feasibility of this kind of silencing in human cancer cells is as yet unknown. The current study was designed to investigate the anti-tumor effects of a homologous promoterless K-ras cDNA system on pancreatic cancer. A full-length K-ras cDNA fragment was cloned into the promoterless plasmid puc19 to yield puc-K-ras. This construct was then transfected into pancreatic cancer cells. Our results demonstrated that the transfection of a promoterless K-ras cDNA resulted in a significant decrease in endogenous K-ras in a dose- and time-dependent manner and induced pancreatic cell apoptosis. Furthermore, stable puc-K-ras transfection decreased the endogenous protein level of K-ras and inhibited cell proliferation, clone formation and tumorigenicity in vivo. These findings indicate a promising application of this homologous promoterless cDNA silencing system in pancreatic cancer gene therapy.

MeSH terms

  • Animals
  • Cell Line, Tumor
  • Cell Proliferation
  • DNA, Complementary / metabolism*
  • Gene Silencing
  • Genetic Therapy / methods
  • Humans
  • Mice
  • Mice, Nude
  • Pancreatic Neoplasms / genetics
  • Pancreatic Neoplasms / metabolism*
  • Plasmids / metabolism
  • Polyethyleneimine / chemistry
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins p21(ras) / genetics*
  • Proto-Oncogene Proteins p21(ras) / metabolism
  • RNA, Small Interfering / metabolism

Substances

  • DNA, Complementary
  • RNA, Small Interfering
  • Polyethyleneimine
  • Proto-Oncogene Proteins p21(ras)