Ribozyme against mutant K-ras mRNA suppresses tumor growth of pancreatic cancer

Int J Oncol. 2004 Mar;24(3):559-64.

Abstract

Point mutations in the K-ras gene are observed at a high incidence in human pancreatic carcinomas. These alterations can be used as potential targets for specific ribozyme-mediated reversal of the malignant phenotype. We designed an anti-K-ras ribozyme against codon 12 of the mutant K-ras gene transcripts (GGT right curved arrow GTT), and generated a recombinant adenovirus to express the ribozyme (rAd/anti-K-ras Rz). We inoculated Capan-1 human pancreatic carcinoma cells in athymic mice, and made Capan-1 tumor xenografts. When the Capan-1 tumors in athymic mice became approximately 100 mm(3), rAd/anti-K-ras Rz was directly injected into the tumor xenografts. Fifteen (68%) of 22 tumors injected with rAd/anti-K-ras Rz showed tumor growth suppression or tumor regression; 6 of 15 tumors were completely regressive, and 1 tumor was recurrent after the tumor regression. By using the recombinant adenovirus in a mice model system, it was possible to accomplish efficient reversion of the malignant phenotype in human pancreatic tumors with K-ras gene mutation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenoviridae / genetics
  • Animals
  • Apoptosis
  • Base Sequence
  • Cell Line, Tumor
  • Codon
  • Genes, ras / genetics*
  • Humans
  • Mice
  • Mice, Nude
  • Molecular Sequence Data
  • Mutation
  • Neoplasm Transplantation
  • Nucleic Acid Conformation
  • Pancreatic Neoplasms / genetics*
  • Pancreatic Neoplasms / therapy
  • Phenotype
  • Point Mutation
  • Polymerase Chain Reaction
  • RNA, Catalytic / genetics
  • RNA, Catalytic / metabolism*
  • RNA, Messenger / metabolism*
  • Time Factors

Substances

  • Codon
  • RNA, Catalytic
  • RNA, Messenger