Beta-catenin, an adherens junction (AJ) protein, was originally identified as a component of cell-cell adhesion structures. AJs are necessary for the creation and maintenance of epithelial cell layers by regulating cell growth and adhesion between cells. Beta-catenin interacts with the cytoplasmic domain of E-cadherin and links E-cadherin to alpha-catenin, which in turn mediates anchorage of the E-cadherin complex to the cortical actin cytoskeleton. Studies show that Beta-catenin also binds to another cytoskeletal complex containing the adenomatous polyposis coli protein and microtubules, and interacts with several signaling pathways that include tyrosine kinases, phosphatases and Wnt/Wingless. The interplay between beta-catenin, cytoskeletal complexes and signaling pathways may regulate morphogenesis. Beta-catenin is expressed in several hair follicle cell types, basal and peripheral matrix cells, and cells of the outer and inner root sheats. A pathological role of beta-catenin has been identified in pilomatrixoma (PTR), medulloblastoma (MDB), colorectal cancer (CRC), ovarian cancer, and tumor development. In the nucleus, beta-catenin serves to co activate a family of Lef/Tcf transcription factors that stimulate transcription of target genes including those encoding cyclin D and c-myc that promote cell proliferation. The influence on cell proliferation is the molecular basis for the role of beta-catenin in tumorgenesis, specifically, solid tumors of the breast, colon, liver, lung, gastric, prostate, and skin.
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