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Cancer Lett. 2013 Nov 28;341(1):41-5. doi: 10.1016/j.canlet.2013.08.027. Epub 2013 Aug 21.

Deadly crosstalk: Notch signaling at the intersection of EMT and cancer stem cells.

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Cancer Institute, University of Mississippi Medical Center, Jackson, MS, United States; Department of Biochemistry, University of Mississippi Medical Center, Jackson, MS, United States.


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.


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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