Endothelin receptor blockade potentiates FasL-induced apoptosis in colon carcinoma cells via the protein kinase C-pathway

Détails

ID Serval
serval:BIB_19F7D762A81E
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Endothelin receptor blockade potentiates FasL-induced apoptosis in colon carcinoma cells via the protein kinase C-pathway
Périodique
Journal of Cardiovascular Pharmacology
Auteur(s)
Eberl  L. P., Egidy  G., Pinet  F., Juillerat-Jeanneret  L.
ISSN
0160-2446 (Print)
Statut éditorial
Publié
Date de publication
2000
Volume
36
Numéro
5 Suppl 1
Pages
S354-S356
Notes
PT - Journal Article PT - Research Support, Non-U.S. Gov't
Résumé
An imbalance between proliferation and apoptosis is important in tumor progression. Endothelin-1 (ET-1) has vasoconstricting and mitogenic activities and may be involved in apoptosis regulation. We found that ET-1 and FasL systems were colocalized in human colon tumors and that ET-1 was secreted by human (HT-29, SW480) and rat (PROb, REGb) colon carcinoma cell lines. Bosentan, a mixed endothelin-A- and -B- (ET(A)/ET(B)) receptor antagonist, potentiated FasL- (APO-1, CD95) induced apoptosis in these cells. The specific inhibition of enzymes involved in ceramide production did not restore survival of cells exposed to FasL and bosentan. Inhibition of PKC with bisindolylmaleimide IX enhanced FasL-induced apoptosis in HT-29, PROb and REGb cells in the absence of bosentan. These results suggest that ET-1 is an autocrine survival factor able to protect colon carcinoma cells against FasL-induced apoptosis, involving the protein kinase C (PKC) but not the sphingomyelin-ceramide signaling transduction pathways
Mots-clé
Animals/Apoptosis/drug effects/Colonic Neoplasms/Pathology/Fas Ligand Protein/Membrane Glycoproteins/physiology/Protein Kinase C/Rats/Receptor,Endothelin A/Receptor,Endothelin B/Receptors,Endothelin/antagonists & inhibitors/Sulfonamides/pharmacology/Tumor Cells,Cultured
Pubmed
Web of science
Création de la notice
29/01/2008 19:35
Dernière modification de la notice
20/08/2019 13:51
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