Baliñas-Gavira, C. (Carlos)

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    Comprehensive Analysis of SWI/SNF Inactivation in Lung Adenocarcinoma Cell Models
    (2020) Patiño-Mercau, J.R. (Juan Rodrigo); Álvarez-Perez, J.C. (Juan Carlos); Romero, O.A. (Octavio A.); Medina, P.P. (Pedro P.); Coira, I.F. (Isabel F.); Cuadros, M. (Marta); Rodriguez, M.I. (Maria Isabel); Arenas, A.M. (Alberto M.); Andrades, A. (Alvaro); Montuenga-Badia, L.M. (Luis M.); Sanjuan-Hidalgo, J. (Juan); Baliñas-Gavira, C. (Carlos); Sanchez-Cespedes, M. (Montserrat); Garcia, D.J. (Daniel J.); Carretero, J. (Julian); Peinado, P. (Paola)
    Mammalian SWI/SNF (SWitch/Sucrose Non-Fermentable) complexes are ATP-dependent chromatin remodelers whose subunits have emerged among the most frequently mutated genes in cancer. Studying SWI/SNF function in cancer cell line models has unveiled vulnerabilities in SWI/SNF-mutant tumors that can lead to the discovery of new therapeutic drugs. However, choosing an appropriate cancer cell line model for SWI/SNF functional studies can be challenging because SWI/SNF subunits are frequently altered in cancer by various mechanisms, including genetic alterations and post-transcriptional mechanisms. In this work, we combined genomic, transcriptomic, and proteomic approaches to study the mutational status and the expression levels of the SWI/SNF subunits in a panel of 38 lung adenocarcinoma (LUAD) cell lines. We found that the SWI/SNF complex was mutated in more than 76% of our LUAD cell lines and there was a high variability in the expression of the different SWI/SNF subunits. These results underline the importance of the SWI/SNF complex as a tumor suppressor in LUAD and the difficulties in defining altered and unaltered cell models for the SWI/SNF complex. These findings will assist researchers in choosing the most suitable cellular models for their studies of SWI/SNF to bring all of its potential to the development of novel therapeutic applications.