Abstract
Blood vessels supply all body tissues with nutrients and oxygen, take away waste products and allow the arrival of immune cells and other cells (pericytes, smooth muscle cells) that form part of these vessels around the principal endothelial cells. Vasculogenic mimicry (VM) is a tumor blood supply system that takes place independently of angiogenesis or endothelial cells, and is associated with poor survival in cancer patients. Aberrant expression of VE-cadherin has been strongly associated with VM. Even more, VE-cadherin has constitutively high phosphorylation levels on the residue of Y658 in human malignant melanoma cells. In this review we focus on non-endothelial VE-cadherin and its post-translational modifications as a crucial component in the development of tumor VM, highlighting the signaling pathways that lead to their pseudo-endothelial and stem-like phenotype and the role of tumor microenvironment. We discuss the importance of the tumor microenvironment in VM acquisition, and describe the most recent therapeutic targets that have been proposed for the repression of VM.
Highlights
The concept of neovascularization was described for the first time in 1787 in the context of developmental biology
VE-cadherin down-regulation leads to the inhibition of Vasculogenic mimicry (VM) formation [19]. In this mini-review, we focus on the new findings on the role of extravascular VE-cadherin and its different localizations in the acquisition of the VM phenotype
All of these functions of VE-PTP have always been studied in endothelial models, though the implications of the vascular endothelial protein tyrosine phosphatase (VEPTP)/VE-cadherin axis in a VM context remain unknown
Summary
The concept of neovascularization was described for the first time in 1787 in the context of developmental biology. Vasculogenic mimicry refers to the ability of cancer cells to organize themselves into vascular-like structures for the obtention of nutrients and oxygen independently of normal blood vessels or angiogenesis. Research in VM has often been surrounded by skepticism to a certain extent The reason for this controversy is usually the difficulty to distinguish VM channels from endothelial blood vessels or blood lakes in vivo. In vitro research presents inherent inconveniences, given the need to develop 3-D models where tumor cells can develop capillary-like structures. The molecular mechanisms that give rise to VM remain largely unknown
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