Targeting SWI/SNF metabolic vulnerabilities in cancer
The SWI/SNF (Switch/Sucrose non-fermentable) complex is a key epigenetic regulator that is conserved across different species. While its functions as a gene expression regulator have been widely characterized, new evidences suggest that it can act as a fundamental modulator of metabolic pathways both in physiological and pathological processes. In this review, we summarized the most recent literature addressing molecular interactions involving members of the SWI/SNF complex and metabolic pathways. We focused on how genetic alterations of SWI/SNF subunits lead to tumorigenesis and aggressive phenotypes during cancer evolution. Finally, we highlighted metabolic vulnerabilities of cancer cells with altered SWI/SNF complex that can be exploited as future clinical targets for the treatment of advanced disease.
SWI/SNF complex is a critical regulator of chromatin accessibility frequently mutated in human cancers. Mutations in the SWI/SNF complex renders cancer cells vulnerable to metabolic perturbations, that may constitute new potential oncological targets.