N-cadherin as a therapeutic target in cancer.

Détails

ID Serval
serval:BIB_325DF6FFC1F2
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
N-cadherin as a therapeutic target in cancer.
Périodique
Expert opinion on investigational drugs
Auteur(s)
Mariotti A., Perotti A., Sessa C., Rüegg C.
ISSN
1744-7658[electronic]
Statut éditorial
Publié
Date de publication
2007
Volume
16
Numéro
4
Pages
451-65
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Review - Publication Status: ppublish
Résumé
During tumor progression, cancer cells undergo dramatic changes in the expression profile of adhesion molecules resulting in detachment from original tissue and acquisition of a highly motile and invasive phenotype. A hallmark of this change, also referred to as the epithelial-mesenchymal transition, is the loss of E- (epithelial) cadherin and the de novo expression of N- (neural) cadherin adhesion molecules. N-cadherin promotes tumor cell survival, migration and invasion, and a high level of its expression is often associated with poor prognosis. N-cadherin is also expressed in endothelial cells and plays an essential role in the maturation and stabilization of normal vessels and tumor-associated angiogenic vessels. Increasing experimental evidence suggests that N-cadherin is a potential therapeutic target in cancer. A peptidic N-cadherin antagonist (ADH-1) has been developed and has entered clinical testing. In this review, the authors discuss the biochemical and functional features of N-cadherin, its potential role in cancer and angiogenesis, and summarize the preclinical and clinical results achieved with ADH-1.
Mots-clé
Animals, Cadherins, Drug Delivery Systems, Humans, Neoplasms, Oligopeptides
Pubmed
Web of science
Création de la notice
28/01/2008 9:34
Dernière modification de la notice
20/08/2019 14:17
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