| Summary: | 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.
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