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http://hdl.handle.net/2445/126451
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DC Field | Value | Language |
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dc.contributor.author | Cufí, Sílvia | - |
dc.contributor.author | Bonavia, Rosa | - |
dc.contributor.author | Vazquez Martin, Alejandro | - |
dc.contributor.author | Oliveras Ferraros, Cristina | - |
dc.contributor.author | Corominas Faja, Bruna | - |
dc.contributor.author | Cuyàs, Elisabet | - |
dc.contributor.author | Martin Castillo, Begoña | - |
dc.contributor.author | Barrajón Catalán, Enrique | - |
dc.contributor.author | Visa, Joana | - |
dc.contributor.author | Segura-Carretero, Antonio | - |
dc.contributor.author | Joven, Jorge | - |
dc.contributor.author | Bosch Barrera, Joaquim | - |
dc.contributor.author | Micol, Vicente | - |
dc.contributor.author | Menendez, Javier A. | - |
dc.date.accessioned | 2018-11-27T08:46:53Z | - |
dc.date.available | 2018-11-27T08:46:53Z | - |
dc.date.issued | 2013-08-21 | - |
dc.identifier.uri | http://hdl.handle.net/2445/126451 | - |
dc.description.abstract | The flavolignan silibinin was studied for its ability to restore drug sensitivity to EGFR-mutant NSCLC xenografts with epithelial-to-mesenchymal transition (EMT)-driven resistance to erlotinib. As a single agent, silibinin significantly decreased the tumor volumes of erlotinib-refractory NSCLC xenografts by approximately 50%. Furthermore, the complete abrogation of tumor growth was observed with the co-treatment of erlotinib and silibinin. Silibinin fully reversed the EMT-related high miR-21/low miR-200c microRNA signature and repressed the mesenchymal markers SNAIL, ZEB, and N-cadherin observed in erlotinib-refractory tumors. Silibinin was sufficient to fully activate a reciprocal mesenchymal-to-epithelial transition (MET) in erlotinib-refractory cells and prevent the highly migratogenic phenotype of erlotinib-resistant NSCLC cells. Given that the various mechanisms of resistance to erlotinib result from EMT, regardless of the EGFR mutation status, a water-soluble, silibinin-rich milk thistle extract might be a suitable candidate therapy for upcoming clinical trials aimed at preventing or reversing NSCLC progression following erlotinib treatment. | - |
dc.format.extent | 10 p. | - |
dc.format.mimetype | application/pdf | - |
dc.language.iso | eng | - |
dc.publisher | Nature Publishing Group | - |
dc.relation.isformatof | Reproducció del document publicat a: https://doi.org/10.1038/srep02459 | - |
dc.relation.ispartof | Scientific Reports, 2013, vol. 3 | - |
dc.relation.uri | https://doi.org/10.1038/srep02459 | - |
dc.rights | cc by (c) Cufí et al., 2013 | - |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | * |
dc.source | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) | - |
dc.subject.classification | Oncogènesi | - |
dc.subject.classification | Càncer de pulmó | - |
dc.subject.other | Carcinogenesis | - |
dc.subject.other | Lung cancer | - |
dc.title | Silibinin suppresses EMT-driven erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivo | - |
dc.type | info:eu-repo/semantics/article | - |
dc.type | info:eu-repo/semantics/publishedVersion | - |
dc.date.updated | 2018-07-24T12:47:04Z | - |
dc.rights.accessRights | info:eu-repo/semantics/openAccess | - |
dc.identifier.pmid | 23963283 | - |
Appears in Collections: | Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL)) |
Files in This Item:
File | Description | Size | Format | |
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CufiiS.pdf | 4.85 MB | Adobe PDF | View/Open |
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