Peinado, PaolaAndrades, AlvaroCuadros, MartaRodriguez, Maria IsabelCoira, Isabel FGarcia, Daniel JÁlvarez-Perez, Juan CarlosBaliñas-Gavira, CarlosArenas, Alberto MPatiño-Mercau, Juan RodrigoSanjuan-Hidalgo, JuanRomero, Octavio AMontuenga, Luis MCarretero, JulianSanchez-Cespedes, MontserratMedina, Pedro P2025-01-072025-01-072020-12-102072-6694https://hdl.handle.net/10668/28417Mammalian 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.enAttribution 4.0 Internationalhttp://creativecommons.org/licenses/by/4.0/SWI/SNF complexcell modelsepigeneticslung adenocarcinomalung cancermulti-omicsresearch article33321963open access10.3390/cancers12123712PMC7763689https://www.mdpi.com/2072-6694/12/12/3712/pdf?version=1607654543https://pmc.ncbi.nlm.nih.gov/articles/PMC7763689/pdf