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dc.contributor.authorSanchez-Alvarez, Miguel 
dc.contributor.authorStrippoli, Raffaele
dc.contributor.authorDonadelli, Massimo
dc.contributor.authorBazhin, Alexandr V
dc.contributor.authorCordani, Marco
dc.date.accessioned2019-10-17T08:01:27Z
dc.date.available2019-10-17T08:01:27Z
dc.date.issued2019-09
dc.identifier.citationCancers (Basel). 2019, 11(10): E1415es_ES
dc.identifier.issn2072-6694es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/8500
dc.description.abstract: The regulation of Reactive Oxygen Species (ROS) levels and the contribution therein from networks regulating cell metabolism, such as autophagy and the mTOR-dependent nutrient-sensing pathway, constitute major targets for selective therapeutic intervention against several types of tumors, due to their extensive rewiring in cancer cells as compared to healthy cells. Here, we discuss the sestrin family of proteins-homeostatic transducers of oxidative stress, and drivers of antioxidant and metabolic adaptation-as emerging targets for pharmacological intervention. These adaptive regulators lie at the intersection of those two priority nodes of interest in antitumor intervention-ROS control and the regulation of cell metabolism and autophagy-therefore, they hold the potential not only for the development of completely novel compounds, but also for leveraging on synergistic strategies with current options for tumor therapy and classification/stadiation to achieve personalized medicine.es_ES
dc.description.sponsorshipThis research was funded by Comunidad de Madrid, grant number IND2017/IND-7809 (to M.C.) and COFUND-IPP (MSCA-CNIC; to M.S.-A.).es_ES
dc.language.isoenges_ES
dc.publisherMultidisciplinary Digital Publishing Institute (MDPI) es_ES
dc.type.hasVersionVoRes_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.subjectROSes_ES
dc.subjectSestrinses_ES
dc.subjectAutophagyes_ES
dc.subjectCancer therapyes_ES
dc.subjectNutrient managementes_ES
dc.subjectStress responsees_ES
dc.titleSestrins as a Therapeutic Bridge between ROS and Autophagy in Canceres_ES
dc.typejournal articlees_ES
dc.rights.licenseAtribución 4.0 Internacional*
dc.identifier.pubmedID31546746es_ES
dc.format.volume11es_ES
dc.format.number10es_ES
dc.format.page1415es_ES
dc.identifier.doi10.3390/cancers11101415es_ES
dc.contributor.funderComunidad de Madrid (España) 
dc.contributor.funderCentro Nacional de Investigaciones Cardiovasculares Carlos III (España) 
dc.description.peerreviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.3390/cancers11101415es_ES
dc.identifier.journalCancerses_ES
dc.repisalud.orgCNICCNIC::Grupos de investigación::Señalización por Integrinases_ES
dc.repisalud.institucionCNICes_ES
dc.rights.accessRightsopen accesses_ES


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