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ΔNp63α and microRNAs: leveraging the epithelial-mesenchymal transition

The epithelial-mesenchymal transition (EMT) is a cellular reprogramming mechanism that is an underlying cause of cancer metastasis. Recent investigations have uncovered an intricate network of regulation involving the TGFβ Wnt, and Notch signaling pathways and small regulatory RNA species called mic...

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Detalles Bibliográficos
Autores principales: Stacy, Andrew J., Craig, Michael P., Sakaram, Suraj, Kadakia, Madhavi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356785/
https://www.ncbi.nlm.nih.gov/pubmed/27924063
http://dx.doi.org/10.18632/oncotarget.13797
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author Stacy, Andrew J.
Craig, Michael P.
Sakaram, Suraj
Kadakia, Madhavi
author_facet Stacy, Andrew J.
Craig, Michael P.
Sakaram, Suraj
Kadakia, Madhavi
author_sort Stacy, Andrew J.
collection PubMed
description The epithelial-mesenchymal transition (EMT) is a cellular reprogramming mechanism that is an underlying cause of cancer metastasis. Recent investigations have uncovered an intricate network of regulation involving the TGFβ Wnt, and Notch signaling pathways and small regulatory RNA species called microRNAs (miRNAs). The activity of a transcription factor vital to the maintenance of epithelial stemness, ?Np63a, has been shown to modulate the activity of these EMT pathways to either repress or promote EMT. Furthermore, ?Np63a is a known regulator of miRNA, including those directly involved in EMT. This review discusses the evidence of ?Np63a as a master regulator of EMT components and miRNA, highlighting the need for a deeper understanding of its role in EMT. This expanded knowledge may provide a basis for new developments in the diagnosis and treatment of metastatic cancer.
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spelling pubmed-53567852017-04-20 ΔNp63α and microRNAs: leveraging the epithelial-mesenchymal transition Stacy, Andrew J. Craig, Michael P. Sakaram, Suraj Kadakia, Madhavi Oncotarget Research Paper The epithelial-mesenchymal transition (EMT) is a cellular reprogramming mechanism that is an underlying cause of cancer metastasis. Recent investigations have uncovered an intricate network of regulation involving the TGFβ Wnt, and Notch signaling pathways and small regulatory RNA species called microRNAs (miRNAs). The activity of a transcription factor vital to the maintenance of epithelial stemness, ?Np63a, has been shown to modulate the activity of these EMT pathways to either repress or promote EMT. Furthermore, ?Np63a is a known regulator of miRNA, including those directly involved in EMT. This review discusses the evidence of ?Np63a as a master regulator of EMT components and miRNA, highlighting the need for a deeper understanding of its role in EMT. This expanded knowledge may provide a basis for new developments in the diagnosis and treatment of metastatic cancer. Impact Journals LLC 2016-12-04 /pmc/articles/PMC5356785/ /pubmed/27924063 http://dx.doi.org/10.18632/oncotarget.13797 Text en Copyright: © 2017 Stacy et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Stacy, Andrew J.
Craig, Michael P.
Sakaram, Suraj
Kadakia, Madhavi
ΔNp63α and microRNAs: leveraging the epithelial-mesenchymal transition
title ΔNp63α and microRNAs: leveraging the epithelial-mesenchymal transition
title_full ΔNp63α and microRNAs: leveraging the epithelial-mesenchymal transition
title_fullStr ΔNp63α and microRNAs: leveraging the epithelial-mesenchymal transition
title_full_unstemmed ΔNp63α and microRNAs: leveraging the epithelial-mesenchymal transition
title_short ΔNp63α and microRNAs: leveraging the epithelial-mesenchymal transition
title_sort δnp63α and micrornas: leveraging the epithelial-mesenchymal transition
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5356785/
https://www.ncbi.nlm.nih.gov/pubmed/27924063
http://dx.doi.org/10.18632/oncotarget.13797
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