Wnt pathways are involved in the control of gene expression, cell behavior, cell adhesion, and cell polarity. The Canonical (β-Catenin-Dependent) Wnt Signaling pathway is the best studied of the Wnt pathways and is highly conserved through evolution. In this pathway, Wnt signaling inhibits the degradation of β-catenin, which can regulate transcription of a number of genes. Wnt signaling is activated via ligation of Wnt proteins to their respective dimeric cell surface receptors composed of the seven transmembrane frizzled proteins and the LRP5/6. Upon ligation to their receptors, the cytoplasmic protein disheveled (Dvl) is recruited, phosphorylated and activated. Activation of Dvl induces the dissociation of GSK-3β from Axin and leads to the inhibition of GSK-3β. Next, the phosphorylation and degradation of β-catenin is inhibited as a result of the inactivation of the "destruction complex". Subsequently, stabilized β-catenin translocates into the nucleus leading to changes in different target gene expressions.
Cancer is a class of diseases in which abnormal cells divide without control and are able to invade other tissues. Cancer cells can spread to other parts of the body through the blood and lymph systems. Normally, cell proliferation is under tight control through many mechanisms. For example, DNA damage and repair mechanisms exist in order to decrease the likelihood of genetic mutation and cell transformation. Apoptosis is needed to destroy cells that represent a threat to the integrity of the organism. In addition, the immune system is ready to recognize and destroy cancerous cells. However these error-correction methods often fail in small ways, especially in environments that make errors more likely to arise and propagate. Accumulating disruptions in these control mechanisms lead to progressive error accumulation until unregulated proliferation and cancer forming.