AI Article Synopsis

  • SWI/SNF chromatin remodeling complexes are often mutated in various human cancers, prompting investigation into their tumor suppressive roles in a genetic model of epithelial tumors.
  • Members of the BAP complex were found to inhibit tumor growth in tissues overexpressing the Yorkie proto-oncogene, but not in those with overactive EGFR.
  • Depleting the BAP complex resulted in increased expression of Yki target genes, as well as upregulation of morphogens like Wingless and Dpp, which together enhance tumor formation alongside Yki.

Article Abstract

Switch/sucrose non-fermentable (SWI/SNF) chromatin remodeling complexes are mutated in many human cancers. In this article, we make use of a genetic model for epithelial tumor formation to explore the tumor suppressive role of SWI/SNF complex proteins. Members of the BAP complex exhibit tumor suppressor activity in tissue overexpressing the Yorkie () proto-oncogene, but not in tissue overexpressing epidermal growth factor receptor (EGFR). The Brahma-associated protein (BAP) complex has been reported to serve as a Yki-binding cofactor to support Yki target expression. However, we observed that depletion of BAP leads to ectopic expression of Yki targets both autonomously and non-autonomously, suggesting additional indirect effects. We provide evidence that BAP complex depletion causes upregulation of the Wingless (Wg) and Decapentaplegic (Dpp) morphogens to promote tumor formation in cooperation with Yki.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5665456PMC
http://dx.doi.org/10.1242/dmm.030122DOI Listing

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