CDH1 and cancer: Metapristone interrupted adhesion of colorectal, breast, ovarian, lung, and melanoma cancer cells to endothelial cells of distant metastasis organ intima.105–109 Pharmacoproteomic analysis uncovered that metapristone intervened the epithelial marker E-cadherin and mesenchymal marker vimentin in breast cancer cells, and built the basis for cancer metastasis chemoprevention.110 Systems pharmacology analysis suggested that metapristone mediated the FAK-Src-Paxillin complex to interfere with heterocellular adhesion.