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Notch signaling: targeting cancer stem cells and epithelial-to-mesenchymal transition
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, the biology of cancer stem cells, tumor angiogenesis, and epithelial-to-mesenchymal transition (EM...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Dove Medical Press
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772757/ https://www.ncbi.nlm.nih.gov/pubmed/24043949 http://dx.doi.org/10.2147/OTT.S36162 |
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author | Espinoza, Ingrid Pochampally, Radhika Xing, Fei Watabe, Kounosuke Miele, Lucio |
author_facet | Espinoza, Ingrid Pochampally, Radhika Xing, Fei Watabe, Kounosuke Miele, Lucio |
author_sort | Espinoza, Ingrid |
collection | PubMed |
description | 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, the biology of cancer stem cells, tumor angiogenesis, and epithelial-to-mesenchymal transition (EMT) have been reported. This review describes the role of Notch in the “stemness” program in cancer cells and in metastases, together with a brief update on the Notch inhibitors currently under investigation in oncology. These agents may be useful in targeting cancer stem cells and to reverse the EMT process. |
format | Online Article Text |
id | pubmed-3772757 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | Dove Medical Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-37727572013-09-16 Notch signaling: targeting cancer stem cells and epithelial-to-mesenchymal transition Espinoza, Ingrid Pochampally, Radhika Xing, Fei Watabe, Kounosuke Miele, Lucio Onco Targets Ther Review 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, the biology of cancer stem cells, tumor angiogenesis, and epithelial-to-mesenchymal transition (EMT) have been reported. This review describes the role of Notch in the “stemness” program in cancer cells and in metastases, together with a brief update on the Notch inhibitors currently under investigation in oncology. These agents may be useful in targeting cancer stem cells and to reverse the EMT process. Dove Medical Press 2013-09-06 /pmc/articles/PMC3772757/ /pubmed/24043949 http://dx.doi.org/10.2147/OTT.S36162 Text en © 2013 Espinoza et al. This work is published by Dove Medical Press Ltd, and licensed under Creative Commons Attribution – Non Commercial (unported, v3.0) License The full terms of the License are available at http://creativecommons.org/licenses/by-nc/3.0/. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Ltd, provided the work is properly attributed. |
spellingShingle | Review Espinoza, Ingrid Pochampally, Radhika Xing, Fei Watabe, Kounosuke Miele, Lucio Notch signaling: targeting cancer stem cells and epithelial-to-mesenchymal transition |
title | Notch signaling: targeting cancer stem cells and epithelial-to-mesenchymal transition |
title_full | Notch signaling: targeting cancer stem cells and epithelial-to-mesenchymal transition |
title_fullStr | Notch signaling: targeting cancer stem cells and epithelial-to-mesenchymal transition |
title_full_unstemmed | Notch signaling: targeting cancer stem cells and epithelial-to-mesenchymal transition |
title_short | Notch signaling: targeting cancer stem cells and epithelial-to-mesenchymal transition |
title_sort | notch signaling: targeting cancer stem cells and epithelial-to-mesenchymal transition |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3772757/ https://www.ncbi.nlm.nih.gov/pubmed/24043949 http://dx.doi.org/10.2147/OTT.S36162 |
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