Related Experiment Video
Updated: Sep 20, 2026
Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis
Published on: March 20, 2026
Importance of vascular endothelial growth factor A in the progression of experimental neuroblastoma
Ulrika Bäckman1, Asa Svensson, Rolf Christofferson
1Department of Medical Cell Biology, Children's Hospital, Uppsala University, Sweden. ulrika.backman@medcellbiol.uu.se
Abstract:
Vascular endothelial growth factor A (VEGF-A) and its receptor tyrosine kinases located on endothelial cells seem to play an important role in the multistep pathway of angiogenesis. SU5416 is a small molecule which inhibits angiogenesis by acting as an inhibitor of VEGF receptor-2 tyrosine kinase. We have developed a reproducible murine model for neuroblastoma, a childhood cancer, based on s.c. xenotransplantation of SH-SY5Y neuroblastoma cells. We found that SH-SY5Y cells expressed VEGF-A on both the mRNA and protein levels, that plasma concentrations of VEGF-A were significantly elevated in animals with neuroblastoma with a volume > 1.4 ml, and that there was a correlation between VEGF-A levels in plasma and tumor size in untreated tumor-bearing animals. Treatment with SU5416 reduced the growth of neuroblastoma tumors by 65% without apparent toxicity. SU5416 treatment also suppressed tumor angiogenesis, despite an increase in plasma VEGF-A levels per ml tumor volume during therapy. Our experimental data suggest that the angiogenesis inhibitor SU5416 may be beneficial in the treatment of solid tumors of childhood such as neuroblastoma.
Insights
The angiogenesis inhibitor SU5416 effectively reduced neuroblastoma tumor growth by 65% in a mouse model. This study highlights SU5416
Area of Science:
- Oncology
- Molecular Biology
- Pharmacology
Background:
- Vascular endothelial growth factor A (VEGF-A) and its receptor tyrosine kinases are crucial for angiogenesis.
- SU5416 is a small molecule inhibitor targeting VEGF receptor-2 tyrosine kinase.
Purpose of the Study:
- To evaluate the efficacy of SU5416 in a murine neuroblastoma model.
- To investigate the effect of SU5416 on tumor growth, angiogenesis, and VEGF-A levels.
Main Methods:
- Developed a reproducible murine neuroblastoma model via subcutaneous xenotransplantation of SH-SY5Y cells.
- Assessed VEGF-A expression at mRNA and protein levels in neuroblastoma cells.
- Measured plasma VEGF-A concentrations in tumor-bearing animals.
- Administered SU5416 treatment and evaluated tumor growth and angiogenesis.
Main Results:
- SH-SY5Y cells express VEGF-A.
- Elevated plasma VEGF-A levels correlated with tumor size in untreated animals.
- SU5416 treatment reduced neuroblastoma tumor growth by 65% without apparent toxicity.
- SU5416 suppressed tumor angiogenesis, even with increased plasma VEGF-A per tumor volume during therapy.
Conclusions:
- SU5416 demonstrates significant anti-tumor activity in a preclinical neuroblastoma model.
- The study suggests SU5416 may be a promising therapeutic agent for childhood solid tumors like neuroblastoma.
- Targeting VEGF receptor-2 with SU5416 effectively inhibits tumor angiogenesis and growth.
