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dc.contributor.authorTornin Cavielles, Juan
dc.contributor.authorMateu Sanz, Miguel
dc.contributor.authorRey, Veronica
dc.contributor.authorMurillo, Dzohara
dc.contributor.authorHuergo García, Carmen
dc.contributor.authorGallego, Borja
dc.contributor.authorRodríguez, Aida
dc.contributor.authorRodríguez, René
dc.contributor.authorCanal Barnils, Cristina
dc.contributor.otherUniversitat Politècnica de Catalunya. Departament de Ciència i Enginyeria de Materials
dc.date.accessioned2023-07-07T11:11:17Z
dc.date.available2023-07-07T11:11:17Z
dc.date.issued2023-06-01
dc.identifier.citationTornín, J. [et al.]. Cold plasma and inhibition of STAT3 selectively target tumorigenicity in osteosarcoma. "Redox Biology", 1 Juny 2023, vol. 62, núm. 102685.
dc.identifier.issn2213-2317
dc.identifier.urihttp://hdl.handle.net/2117/390472
dc.description.abstractOsteosarcoma (OS) is a malignant type of bone cancer that arises in periods of increased bone formation. Curative strategies for these types of tumors have remained essentially unchanged for decades and the overall survival for most advanced cases is still dismally low. This is in part due to the existence of drug resistant Cancer Stem Cells (CSC) with progenitor properties that are responsible for tumor relapse and metastasis. In the quest for therapeutic alternatives for OS, Cold Atmospheric Plasmas and Plasma-Treated Liquids (PTL) have come to the limelight as a source of Reactive Oxygen and Nitrogen Species displaying selectivity towards a variety of cancer cell lines. However, their effects on CSC subpopulations and in vivo tumor growth have been barely studied to date. By employing bioengineered 3D tumor models and in vivo assays, here we show that low doses of PTL increase the levels of pro-stemness factors and the self-renewal ability of OS cells, coupled to an enhanced in vivo tumor growth potential. This could have critical implications to the field. By proposing a combined treatment, our results demonstrate that the deleterious pro-stemness signals mediated by PTL can be abrogated when this is combined with the STAT3 inhibitor S3I-201, resulting in a strong suppression of in vivo tumor growth. Overall, our study unveils an undesirable stem cell-promoting function of PTL in cancer and supports the use of combinatorial strategies with STAT3 inhibitors as an efficient treatment for OS avoiding critical side effects. We anticipate our work to be a starting point for wider studies using relevant 3D tumor models to evaluate the effects of plasma-based therapies on tumor subpopulations of different cancer types. Furthermore, combination with STAT3 inhibition or other suitable cancer type-specific targets can be relevant to consolidate the development of the field.
dc.language.isoeng
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectÀrees temàtiques de la UPC::Enginyeria biomèdica::Biomaterials
dc.subject.lcshPlasma engineering
dc.subject.lcshOsteosarcoma
dc.subject.otherCold atmospheric plasma
dc.subject.otherSTAT3
dc.subject.otherOsteosarcoma
dc.subject.otherCancer stem cells
dc.subject.otherBioengineered model
dc.subject.otherOxidative stress
dc.titleCold plasma and inhibition of STAT3 selectively target tumorigenicity in osteosarcoma
dc.typeArticle
dc.subject.lemacTècniques de plasma
dc.subject.lemacOsteosarcoma
dc.contributor.groupUniversitat Politècnica de Catalunya. BBT - Grup de recerca en Biomaterials, Biomecànica i Enginyeria de Teixits
dc.identifier.doi10.1016/j.redox.2023.102685
dc.description.peerreviewedPeer Reviewed
dc.relation.publisherversionhttps://www.sciencedirect.com/science/article/pii/S2213231723000861
dc.rights.accessOpen Access
local.identifier.drac35660108
dc.description.versionPostprint (published version)
dc.contributor.covenanteeInstitut de Recerca Sant Joan de Déu
dc.contributor.covenanteeHospital Universitario Central de Asturias
dc.contributor.covenanteeInstituto Universitario de Oncología del Principado de Asturias
dc.contributor.covenanteeCIBERONC. Centro de Investigación Biomédica en Red. Cáncer
local.citation.authorTornín, J.; Mateu-Sanz, M.; Rey, V.; Murillo, D.; Huergo, C.; Gallego, B.; Rodríguez, A.; Rodríguez, R.; Canal, C.
local.citation.publicationNameRedox Biology
local.citation.volume62
local.citation.number102685


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