Potential Role of the Tumor Suppressor ADENOMATOUS POLYPOSIS COLI in Polarization of Breast Epithelial Cells
Abstract
Recent evidence suggests that the adenomatous polyposis coli (APC) gene participates in breast tumorigenesis. The APC protein interacts with Beta-catenin and plakoglobin in vivo. Beta-catenin and plakoglobin are components of two specialized anchoring junctions, the adherens junction, a site of attachment for bundles of actin filaments, and the desmosome, a site of attachment for intermediate filaments (e.g., keratin). A direct correlation has been shown between loss of adherens junction components and the metastatic potential of breast cancer. I have used a combination of immunofluorescence microscopy and biochemical fractionation to determine that APC protein is located in the nucleus and the cytoplasm of all breast epithelial cells tested. APC protein concentrated at the edge of breast epithelial cells was eliminated by disruption of keratin filaments and microtubules, but not by actin disruption. APC protein appeared tightly associated with intermediate filaments of the normal breast epithelial cell following sequential extraction. APC was co-immunoprecipitated with keratin but not with actin protein. LiCl-treatment of breast cells led to a delay in both tight and adherens junction formation. These findings are consistent with APC protein interacting with intermediate filaments, but not with actin filaments, and APC protein playing a role in cell polarization.
Document Details
- Document Type
- Technical Report
- Publication Date
- Aug 01, 1999
- Accession Number
- ADA377139
Entities
People
- Kristi Neufield
Organizations
- University of Utah