Potential Role of Chibby as a Tumor Suppressor in Breast Cancer
Abstract
Wnt proteins form a family of highly conserved secreted signaling molecules that regulate cell-cell interactions. Deregulation of Wnt signaling plays a role in breast cancer. Thus, proteins that regulate the activities of Wnt signaling might have a significant impact on oncogenesis. We discovered a novel nuclear protein that antagonizes Beta-catenin-mediated transcriptional activation in mammalian cultured cells. Mechanistically, Chibby competes with TCF to bind to Beta-catenin. Moreover, genetic experiments with the Drosophila Chibby gene indicates that Chibby acts downstream of Drosophila Wnt-1 and upstream of Beta-catenin. Taken together, Chibby represents a conserved nuclear inhibitor of Wnt signaling. The hypothesis of this project was that mutation or alteration of Chibby might lead to hyper-active Wnt signaling and enhance the turmorigenicity or progression of breast cancer. To test this hypothesis, we surveyed a large number of breast cancer samples for mutation or silencing of the Chibby locus. No changes from normal were detected. Thus, our hypothesis may have been incorrect or that loss of Chibby is a rather rare event in breast cancer.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 01, 2005
- Accession Number
- ADA441272
Entities
People
- Richard W. Carthew
Organizations
- Northwestern University