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Glutathione in Ovarian Cancer

2018-06-26Recensão Acesso aberto
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dc.contributor.authorNunes, Sofia C.
dc.contributor.authorSerpa, Jacinta
dc.contributor.authorSerpa, Jacinta
dc.contributor.institutionCentro de Estudos de Doenças Crónicas (CEDOC)
dc.contributor.pblMDPI - Multidisciplinary Digital Publishing Institute
dc.date.accessioned2018-07-06T22:10:56Z
dc.date.available2018-07-06T22:10:56Z
dc.date.issued2018-06-26
dc.descriptionThis research group is supported by Fundação para a Ciência e Tecnologia (FCT) (PhD ProRegeM program, PD/BD/105893/2014, FCT fellowship, PD/BD/105768/2014). iNOVA4Health—UID/Multi/04462/2013, a program financially supported by Fundação para a Ciência e Tecnologia / Ministério da Educação e Ciência, through national funds and co-funded by FEDER under the PT2020 Partnership Agreement is acknowledged.
dc.description.abstractGlutathione (GSH) has several roles in a cell, such as a reactive oxygen species (ROS) scavenger, an intervenient in xenobiotics metabolism and a reservoir of cysteine. All of these activities are important in the maintenance of normal cells homeostasis but can also constitute an advantage for cancer cells, allowing disease progression and resistance to therapy. Ovarian cancer is the major cause of death from gynaecologic disease and the second most common gynaecologic malignancy worldwide. In over 50 years, the overall survival of patients diagnosed with epithelial ovarian cancer has not changed, regardless of the efforts concerning early detection, radical surgery and new therapeutic approaches. Late diagnosis and resistance to therapy are the main causes of this outcome, and GSH is profoundly associated with chemoresistance to platinum salts, which, together with taxane-based chemotherapy and surgery, are the main therapy strategies in ovarian cancer treatment. Herein, we present some insights into the role of GSH in the poor prognosis of ovarian cancer, and also point out how some strategies underlying the dependence of ovarian cancer cells on GSH can be further used to improve the effectiveness of therapy.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent1709297
dc.identifier.doi10.3390/ijms19071882
dc.identifier.otherPURE: 5280572
dc.identifier.otherPURE UUID: d6baa62e-f803-440c-aa75-46b230dd7500
dc.identifier.otherPubMed: 29949936
dc.identifier.otherScopus: 85049138594
dc.identifier.otherWOS: 000442807400061
dc.identifier.urihttp://hdl.handle.net/10362/41061
dc.language.isoeng
dc.peerreviewedyes
dc.relationinfo:eu-repo/grantAgreement/FCT/PD/PD%2FBD%2F105893%2F2014/PT
dc.relationCysteine degradation as a sulfur to sustain oxidative phosphorylation OXPHOS in hypoxic cancer cells - new therapeutic targets.
dc.subjectCancer metabolism
dc.subjectChemoresistance
dc.subjectCysteine
dc.subjectGlutathione
dc.subjectOvarian cancer
dc.subjectPlatinum based drugs
dc.subjectSDG 3 - Good Health and Well-being
dc.titleGlutathione in Ovarian Canceren
dc.title.subtitleA Double-Edged Sworden
dc.typereview
degois.publication.issue7
degois.publication.titleInternational Journal of Molecular Sciences
degois.publication.volume19
dspace.entity.typePublication
oaire.awardNumberPD/BD/105893/2014
oaire.awardTitleCysteine degradation as a sulfur to sustain oxidative phosphorylation OXPHOS in hypoxic cancer cells - new therapeutic targets.
oaire.awardURIinfo:eu-repo/grantAgreement/FCT//PD%2FBD%2F105893%2F2014/PT
person.familyNameSerpa
person.givenNameJacinta
person.identifier.ciencia-id2610-7C0D-38F2
person.identifier.orcid0000-0002-1548-5907
person.identifier.ridO-8942-2014
person.identifier.scopus-author-id6601922586
project.funder.identifierhttp://doi.org/10.13039/501100001871
project.funder.nameFundação para a Ciência e a Tecnologia
rcaap.rightsopenAccess
relation.isAuthorOfPublication5f6eaca2-f01f-4894-8da2-688671913214
relation.isAuthorOfPublication.latestForDiscovery5f6eaca2-f01f-4894-8da2-688671913214
relation.isProjectOfPublicationa6adecd1-aa63-4759-9f77-2530e62c648a
relation.isProjectOfPublication.latestForDiscoverya6adecd1-aa63-4759-9f77-2530e62c648a

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