A candidate for cancer gene therapy: MIP-1 alpha gene transfer to an adenocarcinoma cell line reduced tumorigenicity and induced protective immunity in immunocompetent mice

Pharm Res. 1996 Dec;13(12):1896-901. doi: 10.1023/a:1016057830271.

Abstract

Purpose: To evaluate the possibility of cancer gene therapy by the gene delivery of chemokine, the effects of human macrophage inflammatory protein 1 alpha (hu-MIP-1 alpha), murine-macrophage inflammatory protein 1 alpha (mu-MIP-1 alpha), and human-interleukin 8 (hu-IL-8) on tumor progression and immunization were studied.

Methods: Cachexia-inducing and highly tumorigenic adenocarcinoma cells (cell line colon 26, clone 20) were transfected with either a control plasmid, hu-MIP-1 alpha, mu-MIP-1 alpha, or hu-IL-8 expression vector. The production of hu-MIP-1 alpha reached > 1.5 ng/ml in vitro when transfectant cells were cultured at a cell density of 2 x 10(5) cells in 7 ml for 3 days. Immunocompetent BALB/c mice were inoculated into the footpad with the tumor cells, and then primary tumor growth, morphological analyses, and tumor immunogenicity were studied.

Results: The secretion of hu-MIP-1 alpha, mu-MIP-1 alpha, and hu-IL-8 did not affect the growth rate in vitro. Reduced tumorigenicities in vivo were observed in transfected cells with hu-MIP-1 alpha and mu-MIP-1 alpha. Morphologic observation of the site of inoculation of cells transfected with hu-MIP-1 alpha showed infiltration of macrophages and neutrophils on the 5th day after the inoculation. Mice that had rejected cells transfected with hu-MIP-1 alpha gene were immune to a subsequent challenge with the parental cells.

Conclusions: The rejection of the cells depends on cytolysis and generates potent and long lasting antitumor immunity. These data suggest that tumor cells transfected with the MIP-1 alpha gene might be useful as an effective therapy for the treatment of certain tumors.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adenocarcinoma / genetics
  • Adenocarcinoma / immunology
  • Adenocarcinoma / pathology
  • Adenocarcinoma / therapy*
  • Animals
  • Cachexia
  • Chemokine CCL3
  • Chemokine CCL4
  • Colonic Neoplasms / genetics
  • Colonic Neoplasms / immunology
  • Colonic Neoplasms / pathology
  • Colonic Neoplasms / therapy*
  • Female
  • Gene Transfer Techniques
  • Genetic Therapy*
  • Humans
  • Immunocompetence
  • Interleukin-8 / genetics
  • Lung Neoplasms / secondary
  • Macrophage Inflammatory Proteins / genetics*
  • Mice
  • Mice, Inbred BALB C
  • Neoplasm Transplantation
  • RNA, Messenger / analysis
  • RNA, Neoplasm / analysis
  • Recombinant Proteins / genetics
  • Tumor Cells, Cultured

Substances

  • Chemokine CCL3
  • Chemokine CCL4
  • Interleukin-8
  • Macrophage Inflammatory Proteins
  • RNA, Messenger
  • RNA, Neoplasm
  • Recombinant Proteins