Endothelin receptor type B counteracts tenascin-C-induced endothelin receptor type A-dependent focal adhesion and actin stress fiber disorganization

Détails

ID Serval
serval:BIB_EE9455C4ED47
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Endothelin receptor type B counteracts tenascin-C-induced endothelin receptor type A-dependent focal adhesion and actin stress fiber disorganization
Périodique
Cancer Research
Auteur(s)
Lange  K., Kammerer  M., Hegi  M. E., Grotegut  S., Dittmann  A., Huang  W., Fluri  E., Yip  G. W., Gotte  M., Ruiz  C., Orend  G.
ISSN
0008-5472 (Print)
Statut éditorial
Publié
Date de publication
07/2007
Volume
67
Numéro
13
Pages
6163-73
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Jul 1
Résumé
Tenascin-C, an extracellular matrix molecule of the tumor-specific microenvironment, counteracts the tumor cell proliferation-suppressing effect of fibronectin by blocking the integrin alpha(5)beta(1)/syndecan-4 complex. This causes cell rounding and stimulates tumor cell proliferation. Tenascin-C also stimulates endothelin receptor type A (EDNRA) expression. Here, we investigated whether signaling through endothelin receptors affects tenascin-C-induced cell rounding. We observed that endothelin receptor type B (EDNRB) activation inhibited cell rounding by tenascin-C and induced spreading by restoring expression and function of focal adhesion kinase (FAK), paxillin, RhoA, and tropomyosin-1 (TM1) via activation of epidermal growth factor receptor, phospholipase C, c-Jun NH(2)-terminal kinase, and the phosphatidylinositol 3-kinase pathway. In contrast to EDNRB, signaling through EDNRA induced cell rounding, which correlated with FAK inhibition and TM1 and RhoA protein destabilization in the presence of tenascin-C. This occurred in a mitogen-activated protein kinase/extracellular signal-regulated kinase kinase-dependent manner. Thus, tumorigenesis might be enhanced by tenascin-C involving EDNRA signaling. Inhibition of tenascin-C in combination with blocking both endothelin receptors could present a strategy for sensitization of cancer and endothelial cells toward anoikis.
Mots-clé
Actins/*metabolism Brain Neoplasms/metabolism Cell Adhesion Cell Proliferation Cytoskeleton/metabolism Focal Adhesions *Gene Expression Regulation, Neoplastic Glioma/metabolism Humans Kinetics Receptor, Endothelin A/metabolism/*physiology Receptor, Endothelin B/metabolism/*physiology Signal Transduction Stress Fibers/metabolism Tenascin/*biosynthesis/metabolism
Pubmed
Web of science
Création de la notice
25/01/2008 13:06
Dernière modification de la notice
20/08/2019 16:16
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