Breast cancer antiestrogen resistance 3-p130^Cas interactions promote adhesion disassembly and invasion in breast cancer cells.

ABSTRACT: Adhesion turnover is critical for cell motility and invasion. We previously demonstrated that the adaptor molecule breast cancer antiestrogen resistance 3 (BCAR3) promotes adhesion disassembly and breast tumor cell invasion. One of two established binding partners of BCAR3 is the adaptor molecule, p130^Cas. In this study, we sought to determine whether signaling through the BCAR3-Cas complex was responsible for the cellular functions of BCAR3. We show that the entire pool of BCAR3 is in complex with Cas in invasive breast tumor cells and that these proteins colocalize in dynamic cellular adhesions. Although accumulation of BCAR3 in adhesions did not require Cas binding, a direct interaction between BCAR3 and Cas was necessary for efficient dissociation of BCAR3 from adhesions. Th

SUBMITTER: Cross AM 

PROVIDER: S-EPMC5079856 | biostudies-literature | 2016 Nov

REPOSITORIES: biostudies-literature