Review Article

Plant-Derived Chinese Medicine Monomers on Ovarian Cancer via the Wnt/β-Catenin Signaling Pathway: Review of Mechanisms and Prospects

Figure 1

The Wnt/β-catenin signaling pathway. (a) “Wnt Signaling OFF.” Without Wnt activation, the destruction complex, composed of axin and its tumor suppressor partners APC, GSK-3β, and CK1, is formed. The destruction complex phosphorylates β-catenin and targets it for proteasomal degradation, thus maintaining low levels of β-catenin in the cytoplasm. In addition, the E-cadherin structure includes a C-terminal intracellular domain, a transmembrane hydrophobic domain, and an N-terminal extracellular domain. The C-terminal intracellular domain forms a complex with multiple proteins, including α-catenin, pl20, actin, and β-catenin. E-cadherin can bind β-catenin and fix it on the cell membrane, thus inhibiting β-catenin from entering the nucleus and antagonizing the Wnt signaling pathway. (b) “Wnt Signaling ON”. Wnt binds to Fzd/LRP5/6 receptors triggering the phosphorylation of Dsh, which is a negative regulator of the destruction complex. Dsh then recruits axin, which inhibits the formation of the destruction complex and allows β-catenin to accumulate in the cytoplasm and translocate into the nucleus where it binds to TCF/LEF and activates the transcription of Wnt target genes.