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Related Experiment Video

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Tumor vessel disintegration by maximum tolerable PFKFB3 blockade.

Lena-Christin Conradi1,2, Aleksandra Brajic1,2, Anna Rita Cantelmo1,2

  • 1Laboratory of Angiogenesis and Vascular Metabolism, Department of Oncology, KU Leuven, 3000, Leuven, Belgium.

Angiogenesis
|September 7, 2017
PubMed
Summary

High doses of the PFKFB3 blocker 3PO inhibit tumor growth but damage tumor vasculature, increasing metastasis. Lower doses normalize vessels, reducing cancer spread. Dosing is critical for this anticancer strategy.

Keywords:
AngiogenesisAnti-angiogenic therapyGlycolysisMetabolismPFKFB3

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Area of Science:

  • Biochemistry
  • Oncology
  • Vascular Biology

Background:

  • The glycolytic activator PFKFB3 is crucial for cancer cell metabolism.
  • PFKFB3 blockers are investigated as anticancer agents, with 3PO in phase I clinical trials.
  • Tumor endothelial cells exhibit high glycolytic activity, suggesting potential vascular targets.

Purpose of the Study:

  • To investigate the preclinical effects of a maximum tolerable dose of the PFKFB3 blocker 3PO on tumor vasculature.
  • To compare the effects of high-dose versus low-dose 3PO on tumor growth, vasculature, and metastasis.

Main Methods:

  • Administration of 3PO at maximum tolerable dose (70 mg/kg) and a lower dose (25 mg/kg) in preclinical cancer models.
  • Assessment of tumor growth, endothelial cell proliferation, tumor hypoxia, vascular barrier integrity, and cancer cell dissemination.
  • Evaluation of tumor vessel normalization and maturation.

Main Results:

  • High-dose 3PO (70 mg/kg) inhibited cancer cell proliferation and primary tumor growth.
  • High-dose 3PO caused tumor vessel disintegration, suppressed endothelial cell growth, aggravated hypoxia, and increased vascular leakiness, facilitating metastasis.
  • Low-dose 3PO (25 mg/kg) induced tumor vessel normalization and reduced cancer cell intravasation and metastasis.

Conclusions:

  • The dose of PFKFB3 inhibitors significantly impacts their therapeutic effects on tumor vasculature.
  • High doses may promote metastasis through vascular damage, while lower doses may offer a vessel-normalizing, anti-metastatic effect.
  • Optimizing the dosage of glycolytic inhibitors is essential for effective anticancer treatment and minimizing adverse effects.