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Expression-targeted gene therapy for the treatment of transitional cell carcinoma

X Zhang1, A Atala, W T Godbey

  • 1Department of Chemical and Biomolecular Engineering, Laboratory for Gene Therapy and Cellular Engineering, Lindy Boggs Center, Tulane University, New Orleans, LA 70118, USA.

Cancer Gene Therapy
|March 8, 2008
PubMed

Insights

Targeted gene therapy effectively induced apoptosis in transitional cell carcinomas using a Cox-2 promoter. This novel approach led to significant tumor reduction and remission in mice, showing broad cancer treatment potential.

Area of Science:

  • Oncology
  • Gene Therapy
  • Biochemistry

Background:

  • Transitional cell carcinomas often overexpress cyclooxygenase type 2 (Cox-2).
  • Targeted gene delivery offers a promising strategy for cancer treatment.
  • MB49 cells, a model for carcinomas, exhibit constitutive Cox-2 overexpression.

Purpose of the Study:

  • To investigate targeted gene delivery for inducing apoptosis in transitional cell carcinomas.
  • To evaluate the efficacy of a Cox-2 promoter-driven gene therapy in vivo.
  • To assess the therapeutic potential of inducible caspases for cancer treatment.

Main Methods:

  • In vivo gene delivery to MB49 tumors in mice using plasmids complexed with poly(ethylenimine).
  • Utilized the murine Cox-2 (Tis10) promoter for selective gene expression.
  • Delivered genes encoded inducible forms of caspases 3 and 9, activated by a chemical inducer.

Main Results:

  • Significant reduction in bladder mass and tumor volume observed.
  • Demonstrated anti-angiogenesis and inhibition of tumor growth compared to controls.
  • Achieved complete tumor remission in some cases with no observed bystander effects.

Conclusions:

  • Targeted gene therapy utilizing the Cox-2 promoter is effective in treating transitional cell carcinomas.
  • Inducible caspases offer a controllable mechanism for triggering apoptosis in cancer cells.
  • The broad applicability of this Cox-2 targeted approach suggests potential for treating various Cox-2 overexpressing cancers.

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