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Updated: Apr 28, 2026

Preparation Of Neovascular Tissues from Human Glioma Tissues for Quantitative Proteomics Analysis of Tumor Angiogenesis
Published on: March 20, 2026
Metabolic impact of anti-angiogenic agents on U87 glioma cells
Tanja Mesti1, Philippe Savarin2, Mohamed N Triba2
1Laboratoire de Recherches Biochirurgicales, Université Paris Descartes, Hôpital Européen Georges Pompidou, Paris, France.
Background:
Glioma cells not only secrete high levels of vascular endothelial growth factor (VEGF) but also express VEGF receptors (VEGFR), supporting the existence of an autocrine loop. The direct impact on glioma cells metabolism of drugs targeting the VEGF pathway, such as Bevacizumab (Bev) or VEGFR Tyrosine Kinase Inhibitor (TKI), is poorly known.
Material And Methods:
U87 cells were treated with Bev or SU1498, a selective VEGFR2 TKI. VEGFR expression was checked with FACS flow cytometry and Quantitative Real-Time PCR. VEGF secretion into the medium was assessed with an ELISA kit. Metabolomic studies on cells were performed using High Resolution Magic Angle Spinning Spectroscopy (HR-MAS).
Results:
U87 cells secreted VEGF and expressed low level of VEGFR2, but no detectable VEGFR1. Exposure to SU1498, but not Bev, significantly impacted cell proliferation and apoptosis. Metabolomic studies with HR MAS showed that Bev had no significant effect on cell metabolism, while SU1498 induced a marked increase in lipids and a decrease in glycerophosphocholine. Accordingly, accumulation of lipid droplets was seen in the cytoplasm of SU1498-treated U87 cells.
Conclusion:
Although both drugs target the VEGF pathway, only SU1498 showed a clear impact on cell proliferation, cell morphology and metabolism. Bevacizumab is thus less likely to modify glioma cells phenotype due to a direct therapeutic pressure on the VEGF autocrine loop. In patients treated with VEGFR TKI, monitoring lipids with magnetic resonance spectroscopic (MRS) might be a valuable marker to assess drug cytotoxicity.
Insights
Bevacizumab (Bev) did not impact glioma cell metabolism, unlike VEGFR Tyrosine Kinase Inhibitor (TKI) SU1498, which increased lipids and decreased glycerophosphocholine. SU1498 affected proliferation and apoptosis, suggesting differential drug effects on glioma cells.
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Glioma cells exhibit an autocrine loop involving vascular endothelial growth factor (VEGF) and its receptors (VEGFR).
- The direct metabolic effects of VEGF pathway inhibitors, such as Bevacizumab (Bev) and VEGFR Tyrosine Kinase Inhibitors (TKIs), on glioma cells are not well understood.
Purpose of the Study:
- To investigate the direct impact of Bevacizumab (Bev) and a selective VEGFR2 TKI, SU1498, on glioma cell metabolism and phenotype.
- To compare the efficacy of Bev and SU1498 in targeting the VEGF autocrine loop in glioma cells.
Main Methods:
- U87 glioma cells were treated with Bev or SU1498.
- VEGF and VEGFR expression were analyzed using FACS and qRT-PCR.
- VEGF secretion was measured via ELISA.
- Cellular metabolism was assessed using High Resolution Magic Angle Spinning (HR-MAS) spectroscopy.
Main Results:
- SU1498, but not Bev, significantly affected U87 cell proliferation and apoptosis.
- Metabolomic analysis revealed SU1498 increased lipids and decreased glycerophosphocholine, with visible lipid droplet accumulation.
- Bev showed no significant impact on cell metabolism.
Conclusions:
- SU1498 demonstrates a clear impact on glioma cell proliferation, morphology, and metabolism, unlike Bevacizumab.
- Bevacizumab is less likely to alter glioma cell phenotype through direct pressure on the VEGF autocrine loop.
- Monitoring lipid changes with magnetic resonance spectroscopy (MRS) may serve as a marker for VEGFR TKI cytotoxicity in glioma patients.
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