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Updated: May 10, 2026
A Simple Bioassay for the Evaluation of Vascular Endothelial Growth Factors
Published on: March 15, 2016
Vascular endothelial growth factor as a biomarker for endostatin gene therapy
Marina Souza Braga1, Thiago Lauro Turaça, Karen Foguer
1Nephrology Division, Federal University of Sao Paulo, Sao Paulo, Brazil.
Abstract:
Renal cell carcinoma (RCC) is characterized by high vascular endothelial growth factor (VEGF) production and, consequently, excessive angiogenesis. Several strategies have been developed to target angiogenesis as a method for treating metastatic RCC (mRCC). Endostatin (ES) is a C-terminal fragment of collagen XVIII that has antiangiogenic activity. The aim of this study was to investigate the predictive value of circulating VEGF-A in a murine model of mRCC after ES gene therapy. ES therapy did not affect the levels of collagen XVIII/ES or ES in the tissue. The circulating level of ES was increased in the control and ES-treated groups (normal vs. control, P<0.05 and ES-treated vs. control, P<0.001), and the intratumoral vessels were significantly decreased (ES-treated vs. control, P<0.05). ES therapy decreased the VEGF mRNA levels. The tissue and circulating levels of VEGF in the control group were significantly higher than normal (P<0.01 and P<0.05, respectively). Treatment with ES significantly reduced the VEGF concentrations in both compartments (P<0.001 for tissue and P<0.05 for plasma). Our findings indicate that in addition to the directly targeted tumor vessels, ES exerts its antitumor effect by down-regulating VEGF gene expression in renal tumor cells. Additionally, our findings point to the predictive value of VEGF for ES therapy.
Insights
Endostatin gene therapy reduced tumor blood vessels and vascular endothelial growth factor (VEGF) in a mouse model of metastatic renal cell carcinoma (mRCC). VEGF levels can predict treatment success for endostatin therapy.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Metastatic renal cell carcinoma (mRCC) exhibits high vascular endothelial growth factor (VEGF) production, driving excessive angiogenesis.
- Targeting angiogenesis is a key strategy for treating mRCC.
- Endostatin (ES), a collagen XVIII fragment, possesses antiangiogenic properties.
Purpose of the Study:
- To investigate the predictive value of circulating VEGF-A in a murine model of mRCC following ES gene therapy.
- To assess the impact of ES therapy on VEGF levels and tumor vascularity.
Main Methods:
- Murine model of mRCC treated with ES gene therapy.
- Measurement of tissue and circulating levels of ES and VEGF.
- Assessment of intratumoral vascularity and VEGF mRNA levels.
Main Results:
- ES therapy significantly decreased intratumoral vessels and VEGF mRNA levels.
- Both tissue and plasma VEGF concentrations were significantly reduced by ES treatment.
- Circulating ES levels increased in ES-treated groups compared to controls.
- VEGF levels in control groups were significantly higher than normal.
Conclusions:
- ES exerts its antitumor effect by down-regulating VEGF gene expression in renal tumor cells, in addition to targeting tumor vessels.
- Circulating VEGF serves as a predictive biomarker for ES therapy efficacy in mRCC.
