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Nat Rev Cancer. 2008 Nov;8(11):880-7. doi: 10.1038/nrc2505. Epub 2008 Oct 16.

VEGF-A splicing: the key to anti-angiogenic therapeutics?

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  • 1Microvascular Research Laboratories, Department of Physiology & Pharmacology, Bristol Heart Institute, School of Veterinary Science, University of Bristol, Southwell Street, Bristol BS2 8EJ, UK. s.harper@bristol.ac.uk

Abstract

The physiology of microvessels limits the growth and development of tumours. Tumours gain nutrients and excrete waste through growth-associated microvessels. New anticancer therapies target this microvasculature by inhibiting vascular endothelial growth factor A (VEGF-A) splice isoforms that promote microvessel growth. However, certain VEGF-A splice isoforms in normal tissues inhibit growth of microvessels. Thus, it is the VEGF-A isoform balance, which is controlled by mRNA splicing, that orchestrates angiogenesis. Here, we highlight the functional differences between the pro-angiogenic and the anti-angiogenic VEGF-A isoform families and the potential to harness the synthetic capacity of cancer cells to produce factors that inhibit, rather than aid, cancer growth.

PMID:
18923433
[PubMed - indexed for MEDLINE]
PMCID:
PMC2613352
Free PMC Article

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