Fig. 4

WNT signaling pathways in CRC. Accumulation of secretory Wnt ligands leads to the interaction between FZD and LRP, resulting in the activation of the DVL protein [38]. The DVL is activated and phosphorylated and translocated to the FZD receptor. The β-catenin dissociates from the degradation complex and accumulates in the cytoplasm followed by migration to the nucleus [36]. β-catenin, which is accumulated in the nucleus, could be coupled with TCF or LEF, thereby triggers activating of the expression of target genes involved in pathophysiology of CRC. These target genes are involved in the proliferation and transmission. In the absence of Wnt induction, the cytoplasmic β-catenin exists in the destruction complex, and it is phosphorylated by CK and GSK3β. Subsequently this complex recruits β-TrCP E3 linker and then degrades β-catenin via the proteasome [4]