Vascular permeability changes involved in tumor metastasis

Cancer Lett. 2013 Jul 28;335(2):259-69. doi: 10.1016/j.canlet.2013.03.005. Epub 2013 Mar 14.

Abstract

Cancer cell extravasation resembles the leukocyte recruitment during inflammation. Evidence suggests that cancer cells need to weaken the interendothelial junctions in order to cross the endothelial barrier. Several tumor-derived vasoactive compounds have been pointed out to drive this increase in vascular permeability: VEGF, Angptl4, CCL2, SDF-1, etc. Therefore, tumor cells have a wide repertoire of soluble factors to increase vascular permeability in order to colonize new tissues. Tumor soluble factors activate different signaling pathways to induce interendothelial junction disassembly, one common element is Src kinase. Here we summarize the relevant current knowledge about vascular permeability changes involved in tumor metastasis.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Angiopoietin-Like Protein 4
  • Angiopoietins / metabolism
  • Animals
  • Capillary Permeability*
  • Cell Movement
  • Chemokine CCL2 / metabolism
  • Chemokine CXCL12 / metabolism
  • Endothelial Cells
  • Endothelium, Vascular / metabolism*
  • Humans
  • Intercellular Junctions
  • Mice
  • Neoplasm Metastasis*
  • Neoplasms / blood supply*
  • Neoplasms / pathology
  • Neutrophils / metabolism
  • Signal Transduction
  • Transendothelial and Transepithelial Migration*
  • Vascular Endothelial Growth Factor A / metabolism

Substances

  • ANGPTL4 protein, human
  • Angiopoietin-Like Protein 4
  • Angiopoietins
  • CCL2 protein, human
  • CXCL12 protein, human
  • Chemokine CCL2
  • Chemokine CXCL12
  • Vascular Endothelial Growth Factor A