Signalling pathways in vasculogenic mimicry

Biochim Biophys Acta. 2010 Aug;1806(1):18-28. doi: 10.1016/j.bbcan.2010.01.001. Epub 2010 Jan 14.

Abstract

Solid tumour growth is dependent on the development of an adequate blood supply. For years, sprouting angiogenesis has been considered an exclusive mechanism of tumour vascularization. However, over the last years, several other mechanisms have been identified, including vessel-co-option, intussusception, recruitment of endothelial precursor cells (EPCs) and even mechanisms that do not involve endothelial cells, a process called vasculogenic mimicry (VM). The latter describes a mechanism by which highly aggressive tumour cells can form vessel-like structures themselves, by virtue of their high plasticity. VM has been observed in several tumour types and its occurrence is strongly associated with a poor prognosis. This review will focus on signalling molecules and cascades involved in VM. In addition, we will discuss the presence of VM in relation to ongoing cancer research. Finally, we describe the clinical significance of VM regarding anti-angiogenesis treatment modalities.

Publication types

  • Review

MeSH terms

  • Animals
  • Cyclic AMP / physiology
  • Humans
  • Melanoma / blood supply
  • Neoplasms / blood supply*
  • Neoplastic Stem Cells / physiology
  • Neovascularization, Pathologic / physiopathology*
  • Nodal Signaling Ligands / physiology
  • Proto-Oncogene Proteins / physiology
  • Signal Transduction / physiology*
  • Wnt Proteins / physiology
  • Wnt-5a Protein

Substances

  • Nodal Signaling Ligands
  • Proto-Oncogene Proteins
  • WNT5A protein, human
  • Wnt Proteins
  • Wnt-5a Protein
  • Cyclic AMP