[Frontiers in Bioscience 14, 3094-3110, January 1, 2009]

Crosstalk of VEGF and Notch pathways in tumour angiogenesis: therapeutic implications

Ji-Liang Li, Adrian L. Harris

Cancer Research UK Molecular Oncology Department, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK

TABLE OF CONTENTS

1. Abstract
2. Introduction
3. The VEGF pathway
3.1. VEGF ligands and receptors
3.2. Role in embryonic vascular development
3.3. Role in tumour angiogenesis
4. The Notch pathway
4.1. Notch ligands and receptors
4.2. Role in vascular development and homeostasis
4.3. Role in tumour angiogenesis
5. Interactions between VEGF and Notch pathways
5.1. Genetic interaction
5.2. VEGF induces Notch signalling
5.3. Notch signalling regulates VEGF signalling
5.4. Role in tumour angiogenesis
6. Therapeutic combination by disruption of VEGF and DLL4/Notch pathways
7. Concluding remarks
8. Acknowledgements
9. References

1. ABSTRACT

Angiogenesis is regulated by a number of angiogenic factors through many signalling pathways. The VEGF pathway and Notch signalling are perhaps two of the most important mechanisms in regulation of embryonic vascular development and tumour angiogenesis. Blockade of the VEGF pathway effectively inhibits tumour angiogenesis and growth in preclinical models. The successes in phase III trials have added anti-VEGF agents to standard cancer therapy in several major cancers. A recent flurry of findings indicate that DLL4/Notch signalling decreases angiogenesis by suppressing endothelial tip cell formation; importantly, blockade of DLL4/Notch signalling strikingly increases non-productive angiogenesis but significantly reduces the growth of VEGF-sensitive and VEGF-resistant tumours. The VEGF pathway interplays at several levels with DLL4/Notch signalling in vasculature. VEGF induces DLL4/Notch signalling while DLL4/Notch signalling modulates the VEGF pathway. DLL4 and VEGF emerge to be the yin and yang of angiogenesis. Combination therapy by blocking DLL4/Notch and VEGF pathways synergistically inhibits tumour growth in preclinical models. Thus, targeting the DLL4/Notch pathway, though still at an early stage, may lead to exciting new therapies for clinical application.