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Inhibition of angiogenesis and the angiogenesis/invasion shift

Andreas Bikfalvi1, Michel Moenner, Sophie Javerzat

  • 1University Bordeaux, LAMC, UMR 1029, F-3400 Talence, France. a.bikfalvi@angio.u-bordeaux1.fr

Biochemical Society Transactions
|November 23, 2011
PubMed

Insights

Anti-angiogenesis therapy targeting vascular endothelial growth factor (VEGF) shows limited survival benefits and can promote tumor invasion. New research reveals genes that switch tumors from angiogenic to invasive programs, offering targets for novel therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Therapeutics

Background:

  • Angiogenesis is a key target in cancer therapy, but current strategies, particularly anti-VEGF (vascular endothelial growth factor) treatments, have limitations.
  • Resistance to anti-VEGF therapy is common, and it may paradoxically promote tumor cell invasion and alternative angiogenic pathways like FGFs (fibroblast growth factors).

Purpose of the Study:

  • To identify novel genes upregulated during glioma growth.
  • To investigate the molecular mechanisms by which anti-angiogenesis treatment influences tumor aggressiveness and invasiveness.
  • To explore alternative therapeutic targets independent of VEGF.

Main Methods:

  • Utilized a chick chorioallantoic membrane (CAM) experimental glioma model.
  • Analyzed gene expression changes in response to anti-angiogenesis treatment.
  • Investigated molecular mechanisms driving the switch from angiogenic to invasive tumor programs.

Main Results:

  • Identified novel genes upregulated during glioma growth on the CAM.
  • Demonstrated that anti-angiogenesis treatment in this model upregulates genes associated with glioblastoma aggressiveness.
  • Uncovered a molecular mechanism enabling tumor cells to transition from an angiogenic to an invasive state.

Conclusions:

  • Anti-VEGF therapy can drive tumor aggressiveness by inducing invasive programs.
  • Understanding these molecular switches is crucial for developing more effective cancer treatments.
  • Endogenous molecules offer potential for novel therapeutic and diagnostic tools independent of VEGF.

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