Cadherin was first described by Hyafil and Peyrieras in the 1980s as “Uvomorulin” in mouse and L-CAM in chicken and the mouse gene was later cloned. Many subtypes have since been identified in other species and there are now more than 100 known members in this superfamily.Cadherins can be classified into several subtypes: type I classical cadherins such as E-cadherin, N-cadherin, and P-cadherin.Following are signaling pathways participating in the function of cadherins in cancer. E-cadherin loss lead to the upregulation of β-catenin in cytoplasm and N-cadherin could affect tumorigenesis through interacting with FGFR and stimulating MAPK/ERK pathway.E-cadherin could also activate PI3K-AKT and MEK-ERK pathways. 
N-cadherin activates Ras-MAPK pathway, TCF/LEF transcription factor, etc. P-cadherin could increase tumor migration through interacting with integrin. In endothelial cells, VEGF-VEGFR2 activates VE-cadherin and Src, then leads to VE-cadherin phosphorylation on tyrosines, which would promote endothelial cell proliferation through PI3K/AKT signaling. The Wnt-β-catenin signaling pathway also works in immune cells, which stimulates anti-inflammatory macrophages and tolerogenic DCs. E-cadherin mediates anti-inflammatory activation of macrophages and DCs through PI3K/AKT and NF-κB. Cadherins, vital molecules in tumorigenesis and cancer progression, could be also worked as therapeutic targets in cancer treatment.


1.Weina Yu,et al. Front Oncol. 2019; 9: 989.