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Title: Silibinin suppresses EMT-driven erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivo
Author: Cufí, Sílvia
Bonavia, Rosa
Vazquez Martin, Alejandro
Oliveras Ferraros, Cristina
Corominas Faja, Bruna
Cuyàs, Elisabet
Martin Castillo, Begoña
Barrajón Catalán, Enrique
Visa, Joana
Segura-Carretero, Antonio
Joven, Jorge
Bosch Barrera, Joaquim
Micol, Vicente
Menendez, Javier A.
Keywords: Oncogènesi
Càncer de pulmó
Lung cancer
Issue Date: 21-Aug-2013
Publisher: Nature Publishing Group
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.
Note: Reproducció del document publicat a:
It is part of: Scientific Reports, 2013, vol. 3
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Appears in Collections:Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))

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