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Epigenetic Regulation of the Epithelial to Mesenchymal Transition in Lung Cancer

Lung cancer is the leading cause of cancer deaths worldwide. It is an aggressive and devastating cancer because of metastasis triggered by enhanced migration and invasion, and resistance to cytotoxic chemotherapy. The epithelial to mesenchymal transition (EMT) is a fundamental developmental process...

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Detalles Bibliográficos
Autores principales: Roche, Joëlle, Gemmill, Robert M., Drabkin, Harry A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5532608/
https://www.ncbi.nlm.nih.gov/pubmed/28672805
http://dx.doi.org/10.3390/cancers9070072
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author Roche, Joëlle
Gemmill, Robert M.
Drabkin, Harry A.
author_facet Roche, Joëlle
Gemmill, Robert M.
Drabkin, Harry A.
author_sort Roche, Joëlle
collection PubMed
description Lung cancer is the leading cause of cancer deaths worldwide. It is an aggressive and devastating cancer because of metastasis triggered by enhanced migration and invasion, and resistance to cytotoxic chemotherapy. The epithelial to mesenchymal transition (EMT) is a fundamental developmental process that is reactivated in wound healing and a variety of diseases including cancer where it promotes migration/invasion and metastasis, resistance to treatment, and generation and maintenance of cancer stem cells. The induction of EMT is associated with reprogramming of the epigenome. This review focuses on major mechanisms of epigenetic regulation mainly in lung cancer with recent data on EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit ), the catalytic subunit of the PRC2 (Polycomb Group PcG), that behaves as an oncogene in lung cancer associated with gene repression, non-coding RNAs and the epitranscriptome.
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spelling pubmed-55326082017-08-07 Epigenetic Regulation of the Epithelial to Mesenchymal Transition in Lung Cancer Roche, Joëlle Gemmill, Robert M. Drabkin, Harry A. Cancers (Basel) Review Lung cancer is the leading cause of cancer deaths worldwide. It is an aggressive and devastating cancer because of metastasis triggered by enhanced migration and invasion, and resistance to cytotoxic chemotherapy. The epithelial to mesenchymal transition (EMT) is a fundamental developmental process that is reactivated in wound healing and a variety of diseases including cancer where it promotes migration/invasion and metastasis, resistance to treatment, and generation and maintenance of cancer stem cells. The induction of EMT is associated with reprogramming of the epigenome. This review focuses on major mechanisms of epigenetic regulation mainly in lung cancer with recent data on EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit ), the catalytic subunit of the PRC2 (Polycomb Group PcG), that behaves as an oncogene in lung cancer associated with gene repression, non-coding RNAs and the epitranscriptome. MDPI 2017-06-24 /pmc/articles/PMC5532608/ /pubmed/28672805 http://dx.doi.org/10.3390/cancers9070072 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Roche, Joëlle
Gemmill, Robert M.
Drabkin, Harry A.
Epigenetic Regulation of the Epithelial to Mesenchymal Transition in Lung Cancer
title Epigenetic Regulation of the Epithelial to Mesenchymal Transition in Lung Cancer
title_full Epigenetic Regulation of the Epithelial to Mesenchymal Transition in Lung Cancer
title_fullStr Epigenetic Regulation of the Epithelial to Mesenchymal Transition in Lung Cancer
title_full_unstemmed Epigenetic Regulation of the Epithelial to Mesenchymal Transition in Lung Cancer
title_short Epigenetic Regulation of the Epithelial to Mesenchymal Transition in Lung Cancer
title_sort epigenetic regulation of the epithelial to mesenchymal transition in lung cancer
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5532608/
https://www.ncbi.nlm.nih.gov/pubmed/28672805
http://dx.doi.org/10.3390/cancers9070072
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