Modulation of C6 glioma cell proliferation by ureido calix[8]arenes (Articolo in rivista)

Type
Label
  • Modulation of C6 glioma cell proliferation by ureido calix[8]arenes (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1159/000317518 (literal)
Alternative label
  • Viola S.; Merlo S.; Consoli G. M. L.; Drago F.; Geraci C.; Sortino M.A. (2010)
    Modulation of C6 glioma cell proliferation by ureido calix[8]arenes
    in Pharmacology
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Viola S.; Merlo S.; Consoli G. M. L.; Drago F.; Geraci C.; Sortino M.A. (literal)
Pagina inizio
  • 182 (literal)
Pagina fine
  • 188 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 86 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#pagineTotali
  • 7 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 3 (literal)
Note
  • Scopu (literal)
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • Department of Experimental and Clinical Pharmacology, University of Catania, Viale Doria 6 Catania, Italy; ù Istituto di Chimica Biomolecolare, C.N.R., Via Gaifami 18 Catania, Italy; DISCAFF, University of Piemonte Orientale, Via Bovio 6, Novara, Italy International PhD program in Neuropharmacology (literal)
Titolo
  • Modulation of C6 glioma cell proliferation by ureido calix[8]arenes (literal)
Abstract
  • Calixarenes are synthetic macrocyclic compounds that may serve as scaffolds for biologically active molecules and have been proposed as potential anti-cancer agents. We synthesized a ureido-calix[8]arene carrying N-acetyl-D-glucosamine (GlcNAc) residues (Compound 1) and previously demonstrated it inhibits C6 glioma cell migration and proliferation, with divergent mechanisms. In the present work we explored in more detail the anti-proliferative effect of Compound 1, comparing it to related compounds lacking either the sugar moieties (Compound 2), the multiple ureido groups (Compound 3) or both (Compound 4). Results show that the action of Compound 1 is independent of the GlcNAc residues, requires the presence of multiple ureido groups and does not seem to involve focal adhesion kinase signaling. Inhibition of proliferation is reduced by pre-incubation with EGF and VEGF (20 ng/ml) with Compound 1, and ERK phosphorylation is reduced by treatment with Compound 1 in both basal and EGF-stimulated conditions, suggesting that the observed effect depends on a direct interference with growth factor signaling. (literal)
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