Treatment efficiency of a suicide gene therapy using prostate-specific membrane antigen promoter/enhancer in a castrated mouse model of prostate cancer

Cancer Sci. 2004 Apr;95(4):367-70. doi: 10.1111/j.1349-7006.2004.tb03217.x.

Abstract

Suicide gene therapy has potential for the treatment of prostate cancer under conditions of androgen deprivation. We show here that the combination of promoter/enhancer of prostate-specific membrane antigen (PEPM) and the Cre-loxP system is a good method to express a suicide gene, namely herpes virus thymidine kinase (TK), in prostate cancer cells. We have examined this system in a castration model in vivo, in comparison with a prostate-specific antigen promoter/enhancer system (PP). In the castrated mice, the tumor luciferase activity with the combination of the PEPM plus the Cre-loxP system was about 50 times greater than that with the control GL3 plasmid. A similar increase was observed in non-castrated mice. In contrast, the luciferase activity of the plasmid PP was decreased significantly in tumors from castrated mice as compared with tumors from non-castrated control mice. Regarding the therapeutic effect, the combination plasmid PEPM-Cre plus CMV-loxP-TK exhibited a strong inhibitory effect on tumor growth in the castrated mice, as in the non-castrated mice. In contrast, PP-TK plasmid did not show any significant growth inhibition in the castrated mice. These findings indicate that the combination of PEPM and Cre-loxP system may have a good treatment effect under androgen ablation conditions in vivo, and our system may therefore be applicable to patients who have previously received androgen deprivation therapy.

Publication types

  • Comparative Study

MeSH terms

  • Adenocarcinoma / metabolism
  • Adenocarcinoma / therapy*
  • Animals
  • Antigens, Surface / genetics*
  • Enhancer Elements, Genetic / genetics*
  • Genes, Reporter
  • Genes, Transgenic, Suicide*
  • Genetic Therapy*
  • Genetic Vectors / genetics
  • Glutamate Carboxypeptidase II / genetics*
  • Herpesvirus 1, Human / genetics
  • Humans
  • Liposomes
  • Luciferases / genetics
  • Male
  • Mice
  • Mice, Inbred BALB C
  • Mice, Nude
  • Orchiectomy
  • Promoter Regions, Genetic / genetics*
  • Prostatic Neoplasms / metabolism
  • Prostatic Neoplasms / therapy*
  • Thymidine Kinase / genetics*
  • Xenograft Model Antitumor Assays

Substances

  • Antigens, Surface
  • Liposomes
  • Luciferases
  • Thymidine Kinase
  • FOLH1 protein, human
  • Glutamate Carboxypeptidase II