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Título:	Silibinin suppresses EMT-driven erlotinib resistance by reversing the high miR-21/low miR-200c signature in vivo
Autor/a:	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.
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.
Materia(s):	-Oncogènesi -Càncer de pulmó -Carcinogenesis -Lung cancer
Derechos:	cc by (c) Cufí et al., 2013 http://creativecommons.org/licenses/by/3.0/es/
Tipo de documento:	Artículo Artículo - Versión publicada
Editor:	Nature Publishing Group
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