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Comprehensive Analysis of SWI/SNF Inactivation in Lung Adenocarcinoma Cell Models
Paola Peinado1,2, Alvaro Andrades1,2, Marta Cuadros2,3,4
1Department of Biochemistry and Molecular Biology I, University of Granada, 18071 Granada, Spain.
Abstract:
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.
Insights
SWI/SNF (SWitch/Sucrose Non-Fermentable) complexes are frequently mutated in lung adenocarcinoma (LUAD). This study analyzed SWI/SNF alterations in 38 LUAD cell lines, finding mutations in over 76% and variable subunit expression.
Area of Science:
- Cancer genomics
- Chromatin remodeling
- Molecular oncology
Background:
- Mammalian SWI/SNF complexes are ATP-dependent chromatin remodelers.
- SWI/SNF subunits are among the most frequently mutated genes in cancer.
- SWI/SNF alterations create vulnerabilities exploitable for cancer therapy.
Purpose of the Study:
- To investigate the mutational status and expression of SWI/SNF subunits in lung adenocarcinoma (LUAD) cell lines.
- To characterize the suitability of LUAD cell lines for SWI/SNF functional studies.
- To identify challenges in selecting appropriate cellular models for SWI/SNF research.
Main Methods:
- Genomic, transcriptomic, and proteomic analyses were employed.
- A panel of 38 lung adenocarcinoma (LUAD) cell lines was utilized.
- SWI/SNF subunit alterations and expression levels were comprehensively assessed.
Main Results:
- Over 76% of the analyzed LUAD cell lines exhibited SWI/SNF complex mutations.
- Significant variability was observed in the expression levels of different SWI/SNF subunits.
- The study highlights the complexity of defining SWI/SNF-altered versus unaltered cell models.
Conclusions:
- The SWI/SNF complex functions as a critical tumor suppressor in LUAD.
- Understanding SWI/SNF alterations is crucial for selecting accurate LUAD cell models.
- These findings will aid researchers in developing novel therapeutic strategies targeting SWI/SNF.
