Affiliation:
1. Department of Cellular and Molecular Medicine, University of Copenhagen, Blegdamsvej 3B, Copenhagen 2200N, Denmark
Abstract
SWI/SNF chromatin remodeling complexes are mutated in many human cancers. In this report we make use of a Drosophila 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 (Yki) proto-oncogene, but not in tissue overexpressing EGFR. The 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 and Dpp morphogens to promote tumor formation in cooperation with Yki.
Funder
Novo Nordisk Foundation
Danish council for strategic research
Publisher
The Company of Biologists
Subject
General Biochemistry, Genetics and Molecular Biology,Immunology and Microbiology (miscellaneous),Medicine (miscellaneous),Neuroscience (miscellaneous)
Cited by
13 articles.
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