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Antitumor effects of angiostatin K1-3 and endostatin genes coadministered by the hydrodynamics-based transfection
1Department of Biomedical Laboratory Science, College of Health Science, Yonsei University, Wonju 220-710, Republic of Korea.
Abstract:
Angiostatin and endostatin are potent endothelial cell growth inhibitors and have been carefully evaluated for antiangiogenic cancer therapy. Previously, we have shown that subcutaneous administration of angiostatin K1-3 and endostatin genes complexed with liposomal vectors is a more practical treatment procedure than administration of angiostatin and endostatin proteins. This study provides additional conclusive evidence supporting the effectiveness of antiangiogenic cancer gene therapy employing angiostatin K1-3 and endostatin genes. Plasmids encoding a mouse angiostatin K1-3 gene (pFLAG-AngioK1/3) and an endostatin gene (pFLAG-Endo) were introduced by the hydrodynamic transduction method into mice carrying Matrigel plugs or B16BL6 mouse melanoma tumors. A single systemic injection of the two genes exhibited potent antiangiogenic and antitumor activity in the mouse model. Hydrodynamic coadministration of the genes inhibited the B16BL6 mouse melanoma growth and pulmonary metastasis more effectively than administration of either gene alone. Compared with the untreated control group, the mice cotreated with pFLAG-AngioK1/3 and pFLAG-Endo exhibited 75% reduction of tumor growth while those treated with pFLAG-AngioK1/3 or pFLAG-Endo showed 46% and 52% reduction, respectively. The cotreatment inhibited B16BL6 pulmonary metastasis formation by 80% while the inhibition induced by individual treatment with pFLAG-AngioK1/3 or pFLAG-Endo was 68% and 71%, respectively. These results provide additional evidence that systemic expression of angiostatin K1-3 and/or endostatin genes is a viable alternative procedure for antiangiogenic cancer therapy.
Insights
Gene therapy using angiostatin K1-3 and endostatin genes shows potent antiangiogenic and antitumor effects. Coadministration of these genes significantly reduced tumor growth and metastasis in a mouse model, offering a promising cancer treatment strategy.
Area of Science:
- Oncology
- Gene Therapy
- Molecular Biology
Background:
- Angiostatin and endostatin are known inhibitors of endothelial cell growth.
- Previous studies suggest gene delivery is more practical than protein administration for antiangiogenic therapy.
- This study further validates gene-based antiangiogenic cancer therapy.
Purpose of the Study:
- To provide conclusive evidence for the effectiveness of angiostatin K1-3 and endostatin gene therapy.
- To evaluate the antiangiogenic and antitumor activity of coadministered genes.
- To compare the efficacy of combined gene therapy versus individual gene treatments.
Main Methods:
- Plasmids encoding mouse angiostatin K1-3 and endostatin genes were used.
- Hydrodynamic transduction was employed to introduce the genes into mice.
- Mice models with Matrigel plugs or B16BL6 melanoma tumors were utilized.
Main Results:
- A single systemic injection of both genes demonstrated potent antiangiogenic and antitumor activity.
- Coadministration of angiostatin K1-3 and endostatin genes resulted in a 75% reduction in tumor growth.
- Combined gene therapy inhibited pulmonary metastasis by 80%, outperforming individual gene treatments.
Conclusions:
- Systemic expression of angiostatin K1-3 and endostatin genes is a viable antiangiogenic cancer therapy.
- Hydrodynamic coadministration of these genes offers enhanced antitumor and anti-metastatic effects.
- Gene therapy presents a practical alternative to protein-based antiangiogenic treatments.
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