Chromatin remodeling is a critical step in the DNA damage response, and the ATP-dependent chromatin remodelers are a group of epigenetic regulators that alter nucleosome assembly and regulate transcription factor accessibility to DNA, preventing genomic instability and tumorigenesis caused by DNA damage. The SWI/SNF chromatin remodeling complex is one of them, and mutations in the gene encoding the SWI/SNF subunit are frequently found in digestive tumors. We review the most recent literature on the role of SWI/SNF complexes in digestive tumorigenesis, with different SWI/SNF subunits playing different roles. They regulate the biological behavior of tumor cells, participate in multiple signaling pathways, interact with multiple genes, and have some correlation with the prognosis of patients. Their carcinogenic properties may help discover new therapeutic targets. Understanding the mutations and defects of SWI/SNF complexes, as well as the underlying functional mechanisms, may lead to new strategies for treating the digestive system by targeting relevant genes or modulating the tumor microenvironment.
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ATP-dependent switch/sucrose nonfermenting-type chromatin remodeling complexes (SWI/SNF CRCs) are multiprotein machineries altering chromatin structure, thus controlling the accessibility of genomic DNA to various regulatory proteins including transcription factors (TFs). SWI/SNF CRCs are highly evolutionarily conserved among eukaryotes. There are three main subtypes of SWI/SNF CRCs: canonical (cBAF), polybromo (pBAF), and noncanonical (ncBAF) in humans and their functional Arabidopsis counterparts SYD-associated SWI/SNF (SAS), MINU-associated SWI/SNF (MAS), and BRAHMA (BRM)-associated SWI/SNF (BAS).
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