Potential Role of the Tumor Suppressor ADENOMATOUS POLYPOSIS COLI in Polarization of Breast Epithelial Cells

摘要

Recent evidence suggests that the adenomatous polyposis coli (APC) gene participates in breast tumorigenesis. 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.