| Literature DB >> 23973264 |
Ingrid Espinoza1, Lucio Miele.
Abstract
Notch signaling is an evolutionarily conserved pathway involved in cell fate control during development, stem cell self-renewal and postnatal tissue differentiation. Roles for Notch in carcinogenesis, in the biology of cancer stem cells, tumor angiogenesis and epithelial-to-mesenchymal transition (EMT) have been reported. This mini-review describes the role of Notch signaling deregulation in EMT and tumor aggressiveness. We describe how accumulated evidence suggests that Notch inhibition is an attractive strategy for the treatment of several cancers, at least in part because of its potential to reverse or prevent EMT. Published by Elsevier Ireland Ltd.Entities:
Keywords: A Disintegrin And Metalloprotease 10/17; ADAM10/17; CBF-1, Suppressor of Hairless/LAG1; CSCs; CSL; Cancer stem cells; EGFR; EMT; EndMT; Hedgehog; Hh; N(EC); N(IC); N(TM); NF-κB; NO Synthase; Notch extracellular domain; Notch inhibitors; Notch intracellular domain; Notch signaling; Notch transmembrane domain; Oxide Nitric Synthase; PDGF-D; Platelet-derived growth factor D; TGF-β; Tie1-2; Transforming growth factor beta; Tyrosine kinase with immunoglobulin-like and EGF-like domains 1-2; VE-cadherin; VEGF; Vascular Endothelial Growth Factor; Vascular endothelial cadherin; ZEB1; Zinc finger E-box-binding homeobox 1; cancer stem cells; endothelial mesenchymal transition; epidermal growth factor receptor; epithelial mesenchymal transition; nuclear factor kappa-light-chain-enhancer of activated B cells
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Year: 2013 PMID： 23973264 DOI： 10.1016/j.canlet.2013.08.027
Source DB: PubMed Journal: Cancer Lett ISSN： 0304-3835 Impact factor: 8.679