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Epigenetic Control of Autophagy in Cancer Cells: A Key Process for Cancer-Related Phenotypes

Although autophagy is a well-known and extensively described cell pathway, numerous studies have been recently interested in studying the importance of its regulation at different molecular levels, including the translational and post-translational levels. Therefore, this review focuses on the links...

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Autores principales: Peixoto, Paul, Grandvallet, Céline, Feugeas, Jean-Paul, Guittaut, Michaël, Hervouet, Eric
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6952790/
https://www.ncbi.nlm.nih.gov/pubmed/31861179
http://dx.doi.org/10.3390/cells8121656
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author Peixoto, Paul
Grandvallet, Céline
Feugeas, Jean-Paul
Guittaut, Michaël
Hervouet, Eric
author_facet Peixoto, Paul
Grandvallet, Céline
Feugeas, Jean-Paul
Guittaut, Michaël
Hervouet, Eric
author_sort Peixoto, Paul
collection PubMed
description Although autophagy is a well-known and extensively described cell pathway, numerous studies have been recently interested in studying the importance of its regulation at different molecular levels, including the translational and post-translational levels. Therefore, this review focuses on the links between autophagy and epigenetics in cancer and summarizes the. following: (i) how ATG genes are regulated by epigenetics, including DNA methylation and post-translational histone modifications; (ii) how epidrugs are able to modulate autophagy in cancer and to alter cancer-related phenotypes (proliferation, migration, invasion, tumorigenesis, etc.) and; (iii) how epigenetic enzymes can also regulate autophagy at the protein level. One noteable observation was that researchers most often reported conclusions about the regulation of the autophagy flux, following the use of epidrugs, based only on the analysis of LC3B-II form in treated cells. However, it is now widely accepted that an increase in LC3B-II form could be the consequence of an induction of the autophagy flux, as well as a block in the autophagosome-lysosome fusion. Therefore, in our review, all the published results describing a link between epidrugs and autophagy were systematically reanalyzed to determine whether autophagy flux was indeed increased, or inhibited, following the use of these potentially new interesting treatments targeting the autophagy process. Altogether, these recent data strongly support the idea that the determination of autophagy status could be crucial for future anticancer therapies. Indeed, the use of a combination of epidrugs and autophagy inhibitors could be beneficial for some cancer patients, whereas, in other cases, an increase of autophagy, which is frequently observed following the use of epidrugs, could lead to increased autophagy cell death.
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spelling pubmed-69527902020-01-23 Epigenetic Control of Autophagy in Cancer Cells: A Key Process for Cancer-Related Phenotypes Peixoto, Paul Grandvallet, Céline Feugeas, Jean-Paul Guittaut, Michaël Hervouet, Eric Cells Review Although autophagy is a well-known and extensively described cell pathway, numerous studies have been recently interested in studying the importance of its regulation at different molecular levels, including the translational and post-translational levels. Therefore, this review focuses on the links between autophagy and epigenetics in cancer and summarizes the. following: (i) how ATG genes are regulated by epigenetics, including DNA methylation and post-translational histone modifications; (ii) how epidrugs are able to modulate autophagy in cancer and to alter cancer-related phenotypes (proliferation, migration, invasion, tumorigenesis, etc.) and; (iii) how epigenetic enzymes can also regulate autophagy at the protein level. One noteable observation was that researchers most often reported conclusions about the regulation of the autophagy flux, following the use of epidrugs, based only on the analysis of LC3B-II form in treated cells. However, it is now widely accepted that an increase in LC3B-II form could be the consequence of an induction of the autophagy flux, as well as a block in the autophagosome-lysosome fusion. Therefore, in our review, all the published results describing a link between epidrugs and autophagy were systematically reanalyzed to determine whether autophagy flux was indeed increased, or inhibited, following the use of these potentially new interesting treatments targeting the autophagy process. Altogether, these recent data strongly support the idea that the determination of autophagy status could be crucial for future anticancer therapies. Indeed, the use of a combination of epidrugs and autophagy inhibitors could be beneficial for some cancer patients, whereas, in other cases, an increase of autophagy, which is frequently observed following the use of epidrugs, could lead to increased autophagy cell death. MDPI 2019-12-17 /pmc/articles/PMC6952790/ /pubmed/31861179 http://dx.doi.org/10.3390/cells8121656 Text en © 2019 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
Peixoto, Paul
Grandvallet, Céline
Feugeas, Jean-Paul
Guittaut, Michaël
Hervouet, Eric
Epigenetic Control of Autophagy in Cancer Cells: A Key Process for Cancer-Related Phenotypes
title Epigenetic Control of Autophagy in Cancer Cells: A Key Process for Cancer-Related Phenotypes
title_full Epigenetic Control of Autophagy in Cancer Cells: A Key Process for Cancer-Related Phenotypes
title_fullStr Epigenetic Control of Autophagy in Cancer Cells: A Key Process for Cancer-Related Phenotypes
title_full_unstemmed Epigenetic Control of Autophagy in Cancer Cells: A Key Process for Cancer-Related Phenotypes
title_short Epigenetic Control of Autophagy in Cancer Cells: A Key Process for Cancer-Related Phenotypes
title_sort epigenetic control of autophagy in cancer cells: a key process for cancer-related phenotypes
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6952790/
https://www.ncbi.nlm.nih.gov/pubmed/31861179
http://dx.doi.org/10.3390/cells8121656
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