Alternative splicing in angiogenesis: The vascular endothelial growth factor paradigm

Ladomery, Michael; Harper, Steven J.; Bates, David O.

Abstract

Alternative splicing, first discovered in the 1970s, has emerged as one of the key generators of proteomic diversity. Not surprisingly, alternative splicing is increasingly linked to the etiology of cancer. This is illustrated by vascular endothelial growth factor (VEGF), the dominant angiogenic factor. Recently, an antiangiogenic family of VEGF isoforms was discovered, and termed VEGF xxx b. VEGF xxx b isoforms arise from an alternative 3′ splice site in exon 8, and differ by a mere six amino acids at the C-terminus. These alternative six amino acids radically change the functional properties of VEGF. VEGF xxx b isoform expression is regulated in human tissues and development, and disregulated in many pathological states including cancer. Understanding what regulates VEGF xxx b alternative splicing, and therefore the balance of pro- and antiangiogenic isoforms is of great importance and will be explored in detail over the next few years. © 2006 Elsevier Ireland Ltd. All rights reserved.

• Journal Article Type: Short Survey
• Publication Date: May 8, 2007
• Journal: Cancer Letters
• Print ISSN: 0304-3835
• Publisher: Elsevier
• Peer Reviewed: Peer Reviewed
• Volume: 249
• Issue: 2
• Pages: 133-142
• DOI: https://doi.org/10.1016/j.canlet.2006.08.015
• Keywords: alternative splicing, VEGF, angiogenesis, tumors, VEGF165b
• Public URL: https://uwe-repository.worktribe.com/output/1027890
• Publisher URL: http://dx.doi.org/10.1016/j.canlet.2006.08.015