ARID1A loss impairs enhancer-mediated gene regulation and drives colon cancer in mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-02

AUTHORS

Radhika Mathur, Burak H Alver, Adrianna K San Roman, Boris G Wilson, Xiaofeng Wang, Agoston T Agoston, Peter J Park, Ramesh A Shivdasani, Charles W M Roberts

ABSTRACT

Genes encoding subunits of SWI/SNF (BAF) chromatin-remodeling complexes are collectively mutated in ∼20% of all human cancers. Although ARID1A is the most frequent target of mutations, the mechanism by which its inactivation promotes tumorigenesis is unclear. Here we demonstrate that Arid1a functions as a tumor suppressor in the mouse colon, but not the small intestine, and that invasive ARID1A-deficient adenocarcinomas resemble human colorectal cancer (CRC). These tumors lack deregulation of APC/β-catenin signaling components, which are crucial gatekeepers in common forms of intestinal cancer. We find that ARID1A normally targets SWI/SNF complexes to enhancers, where they function in coordination with transcription factors to facilitate gene activation. ARID1B preserves SWI/SNF function in ARID1A-deficient cells, but defects in SWI/SNF targeting and control of enhancer activity cause extensive dysregulation of gene expression. These findings represent an advance in colon cancer modeling and implicate enhancer-mediated gene regulation as a principal tumor-suppressor function of ARID1A. More... »

PAGES

296-302

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ng.3744

DOI

http://dx.doi.org/10.1038/ng.3744

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1013224156

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27941798


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