β-Catenin, a multifunctional protein, was originally identified as a component of cell–cell adhesion machinery. β-Catenin-mediated signaling, which regulates developmental processes, may act as a potential link between inflammation and cancer. The protein β-catenin is an essential component of intercellular junctions and the Wnt growth factor signaling pathway.
In many cancers, mutation of Wnt pathway components leads to activation of oncogenes by β-catenin–TCF transcription factor complex. Disruption of β-catenin-mediated TCF signaling is a promising strategy for early chemopreventive intervention. The mechanism by which agents disrupt β-catenin-mediated TCF signaling is not completely known; however, some mechanisms have been suggested. They include: (1) physical inhibition of the β-catenin/TCF complex formation, (2) upregulation of the ubiquitin-mediated proteosomal degradation of β-catenin, (3) accelerated the nuclear export of β-catenin, and (4) enhanced sequestration of β-catenin by E-cadherin.
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