Fiche publication
Date publication
décembre 2019
Journal
Cells
Auteurs
Membres identifiés du Cancéropôle Est :
Pr GUITTAUT Michaël
,
Dr HERVOUET Eric
,
Dr PEIXOTO Paul
,
Pr FEUGEAS Jean-Paul
Tous les auteurs :
Peixoto P, Grandvallet C, Feugeas JP, Guittaut M, Hervouet E
Lien Pubmed
Résumé
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 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.
Mots clés
DNA methylation, autophagy, cancer, epigenetics, histone deacetylase (HDAC), histone methylation
Référence
Cells. 2019 Dec 17;8(12):
