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Adipocyte secretome increases radioresistance of malignant melanocytes by improving cell survival and decreasing oxidative status

dc.contributor.authorCoelho, Pedro
dc.contributor.authorSilva, Liliana
dc.contributor.authorFaria, Isabel
dc.contributor.authorVieira, Mónica
dc.contributor.authorMonteiro, Armanda
dc.contributor.authorPinto, Gabriela
dc.contributor.authorPrudêncio, Cristina
dc.contributor.authorFernandes, Rúben
dc.contributor.authorSoares, Raquel
dc.date.accessioned2021-11-22T13:56:04Z
dc.date.available2021-11-22T13:56:04Z
dc.date.issued2017-05-01
dc.description.abstractRadiotherapy is a treatment option for the majority of malignancies. However, because melanoma is known to be radioresistant, the use of ionizing radiation as an adjuvant therapy in cutaneous melanoma patients is ineffective. Obesity has now been recognized as a risk factor for melanoma. High adiposity is generally associated with a more pro-oxidative status. Oxidative stress is a major player in radiation therapy and also a common link between obesity and cancer. Several adipocyte-released proteins are known to have a role in controlling cellular growth and pro-survival signaling. For that reason, we investigated the influence of 3T3-L1 mature adipocyte secretome in B16-F10 malignant melanocyte radiosensitivity. We evaluated B16-F10 cell survival and redox homeostasis when exposed to four daily doses of ionizing radiation (2 Gy per day) up to a total of 8 Gy in a medical linear accelerator. B16-F10 melanocytes exhibited slight alterations in survival, catalase activity, nitrative stress and total oxidant concentration after the first 2 Gy irradiation. The motility of the melanocytes was also delayed by ionizing radiation. Subsequent irradiations of the malignant melanocytes led to more prominent reductions in overall survival. Remarkably, 3T3-L1 adipocyte-secreted molecules were able to increase the viability and migration of melanocytes, as well as lessen the pro-oxidant burden induced by both the single and cumulative X-ray doses. In vitro adipocyte-released factors protected B16-F10 malignant melanocytes from both oxidative stress and loss of viability triggered by radiation, enhancing the radioresistant phenoyype of these cells with a concomitant activation of the AKT signaling pathway These results both help to elucidate how obesity influences melanoma radioresistance and support the usage of conventional medical linear accelerators as a valid model for the in vitro radiobiological study of tumor cell lines.pt_PT
dc.description.versioninfo:eu-repo/semantics/publishedVersionpt_PT
dc.identifier.citationCoelho, P., Silva, L., Faria, I., Vieria, M., Monteiro, A., Pinto, G., Prudêncio, C., Fernandes, R., & Soares, R. (2017). Adipocyte Secretome Increases Radioresistance of Malignant Melanocytes by Improving Cell Survival and Decreasing Oxidative Status. Radiation Research, 187(5), 581-588. https://doi.org/10.1667/rr14551.1pt_PT
dc.identifier.doi10.1667/RR14551.1pt_PT
dc.identifier.eissn1938-5404
dc.identifier.urihttp://hdl.handle.net/10400.22/18926
dc.language.isoengpt_PT
dc.peerreviewedyespt_PT
dc.publisherRadiation Research Societypt_PT
dc.relation.publisherversionhttps://meridian.allenpress.com/radiation-research/article-abstract/187/5/581/150723/Adipocyte-Secretome-Increases-Radioresistance-of?redirectedFrom=fulltextpt_PT
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/pt_PT
dc.subjectAdipocyte secretomept_PT
dc.subjectMalignant melanocytespt_PT
dc.titleAdipocyte secretome increases radioresistance of malignant melanocytes by improving cell survival and decreasing oxidative statuspt_PT
dc.typejournal article
dspace.entity.typePublication
oaire.citation.endPage588pt_PT
oaire.citation.startPage581pt_PT
oaire.citation.titleRadiation Researchpt_PT
oaire.citation.volume187pt_PT
person.familyNameCoelho
person.familyNameFaria
person.familyNameVieira
person.familyNamePrudêncio
person.familyNameFernandes
person.givenNamePedro
person.givenNameIsabel
person.givenNameMónica
person.givenNameCristina
person.givenNameRúben
person.identifier1200571
person.identifier.ciencia-idBE18-3DB2-8D79
person.identifier.ciencia-idC81E-F4EE-FADE
person.identifier.orcid0000-0002-2343-1108
person.identifier.orcid0000-0003-2207-7503
person.identifier.orcid0000-0002-9614-9031
person.identifier.orcid0000-0002-9920-936X
person.identifier.orcid0000-0002-9914-4965
person.identifier.ridAAZ-9239-2020
person.identifier.ridD-8977-2016
person.identifier.scopus-author-id57214054449
person.identifier.scopus-author-id24464652500
person.identifier.scopus-author-id6508057930
rcaap.rightsopenAccesspt_PT
rcaap.typearticlept_PT
relation.isAuthorOfPublicationeb030614-4140-437b-8ac3-f59c52566ecf
relation.isAuthorOfPublicationf8724d1d-fd77-4730-8d6c-6f55ee55a07f
relation.isAuthorOfPublication55587c4b-3df0-4ff1-bade-587420940ecd
relation.isAuthorOfPublication881a8ad5-ab13-4e49-89f4-08ca61cc81e3
relation.isAuthorOfPublication673a8adb-7876-47d7-98c4-2cd502da4ed4
relation.isAuthorOfPublication.latestForDiscovery881a8ad5-ab13-4e49-89f4-08ca61cc81e3

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