When the endothelium scores an own goal: Endothelial cells actively augment metastatic extravasation through endothelial-mesenchymal transition

Ákos Gasparics, L. Rosivall, I. Krizbai, Attila Sebe

Research output: Contribution to journalReview article

17 Citations (Scopus)

Abstract

Endothelial-mesenchymal transition (EndMT) is an important mechanism during organ development and in certain pathological conditions. For example, EndMT contributes to myofibroblast formation during organ fibrosis, and it has been identified as an important source of cancer-associated fibroblasts, facilitating tumor progression. Recently, EndMT was proposed to modulate endothelial function during intravasation and extravasation of metastatic tumor cells. Evidence suggests that endothelial cells are not passive actors during transendothelial migration (TEM) of cancer cells, as there are profound changes in endothelial junctional protein expression, signaling, permeability, and contractility. This review describes these alterations in endothelial characteristics during TEM of metastatic tumor cells and discusses them in the context of EndMT. EndMT could play an important role during metastatic intravasation and extravasation, a novel hypothesis that may lead to new therapeutic approaches to tackle metastatic disease.

Original languageEnglish
Pages (from-to)H1055-H1062
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume310
Issue number9
DOIs
Publication statusPublished - May 1 2016

Fingerprint

Endothelium
Endothelial Cells
Transendothelial and Transepithelial Migration
Neoplasms
Myofibroblasts
Permeability
Fibrosis
Proteins
Therapeutics

Keywords

  • Endothelial-mesenchymal transition
  • Metastatic extravasation
  • Transendothelial migration

ASJC Scopus subject areas

  • Physiology
  • Medicine(all)
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

Cite this

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AU - Sebe, Attila

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N2 - Endothelial-mesenchymal transition (EndMT) is an important mechanism during organ development and in certain pathological conditions. For example, EndMT contributes to myofibroblast formation during organ fibrosis, and it has been identified as an important source of cancer-associated fibroblasts, facilitating tumor progression. Recently, EndMT was proposed to modulate endothelial function during intravasation and extravasation of metastatic tumor cells. Evidence suggests that endothelial cells are not passive actors during transendothelial migration (TEM) of cancer cells, as there are profound changes in endothelial junctional protein expression, signaling, permeability, and contractility. This review describes these alterations in endothelial characteristics during TEM of metastatic tumor cells and discusses them in the context of EndMT. EndMT could play an important role during metastatic intravasation and extravasation, a novel hypothesis that may lead to new therapeutic approaches to tackle metastatic disease.

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