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Potential of Melatonin as Adjuvant Therapy of Oral Cancer in the Era of Epigenomics

dc.contributor.authorCapote-Moreno, Ana
dc.contributor.authorRamos Alonso, Eva
dc.contributor.authorEgea, Javier
dc.contributor.authorLópez-Muñoz, Francisco
dc.contributor.authorGil-Martín, Emilio
dc.contributor.authorRomero Martínez, Manuel Alejandro
dc.date.accessioned2023-06-17T09:00:56Z
dc.date.available2023-06-17T09:00:56Z
dc.date.issued2019-11-02
dc.description.abstractThe wide variety of epigenetic controls available is rapidly expanding the knowledge of molecular biology even overflowing it. At the same time, it can illuminate unsuspected ways of understanding the etiology of cancer. New emerging therapeutic horizons, then, promise to overcome the current antitumor strategies need. The translational utility of this complexity is particularly welcome in oral cancer (OC), in which natural history is alarmingly disappointing due to the invasive and mutilating surgery, the high relapsing rate, the poor quality of life and the reduced survival after diagnosis. Melatonin activates protective receptor-dependent and receptor-independent processes that prevent tissue cancerisation and inhibit progressive tumor malignancy and metastasis. Related evidence has shown that melatonin pleiotropy encompasses gene expression regulation through all the three best-characterized epigenetic mechanisms: DNA methylation, chromatin modification, and non-coding RNA. OC has received less attention than other cancers despite prognosis is usually negative and there are no significant therapy improvements recorded in the past decade. However, a large research effort is being carried out to elucidate how melatonin´s machinery can prevent epigenetic insults that lead to cancer. In the light of recent findings, a comprehensive examination of biochemistry through which melatonin may reverse epigenetic aberrations in OC is an extraordinary opportunity to take a step forward in the clinical management of patients.
dc.description.departmentSección Deptal. de Farmacología y Toxicología (Veterinaria)
dc.description.facultyFac. de Veterinaria
dc.description.refereedTRUE
dc.description.sponsorshipInstituto de Salud Carlos III (ISCIII)/FEDER
dc.description.statuspub
dc.eprint.idhttps://eprints.ucm.es/id/eprint/64484
dc.identifier.doi10.3390/cancers11111712
dc.identifier.issn2072-6694
dc.identifier.officialurlhttps://doi.org/10.3390/cancers11111712
dc.identifier.relatedurlhttps://www.mdpi.com/2072-6694/11/11/1712
dc.identifier.urihttps://hdl.handle.net/20.500.14352/7929
dc.issue.number11
dc.journal.titleCancers
dc.language.isoeng
dc.page.initial1712
dc.publisherMDPI
dc.relation.projectID(Programa Miguel Servet CP14/00008; PI16/00735)
dc.rightsAtribución 3.0 España
dc.rights.accessRightsopen access
dc.rights.urihttps://creativecommons.org/licenses/by/3.0/es/
dc.subject.keywordoral cancer
dc.subject.keywordmelatonin
dc.subject.keywordadjuvant treatment
dc.subject.keywordmelatonin receptors
dc.subject.keywordepigenetics
dc.subject.keywordmethylation
dc.subject.keywordchromatin modification
dc.subject.keywordmiRNAs
dc.subject.ucmOncología
dc.subject.ucmMicrobiología (Veterinaria)
dc.subject.unesco3201.01 Oncología
dc.subject.unesco3109.05 Microbiología
dc.titlePotential of Melatonin as Adjuvant Therapy of Oral Cancer in the Era of Epigenomics
dc.typejournal article
dc.volume.number11
dspace.entity.typePublication
relation.isAuthorOfPublication5f16335c-a2b9-4244-b00f-215f16e7150c
relation.isAuthorOfPublicationc658be58-bda9-4100-ad65-bac31e1256af
relation.isAuthorOfPublication.latestForDiscovery5f16335c-a2b9-4244-b00f-215f16e7150c

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