FOCUS on New Drug Targets: Epithelial-to-mesenchymal (EMT) transition is widely recognized as a cell-intrinsic process that augments the metastatic potential of cancer cells by enhancing motility and invasiveness. In a paper just out in PNAS, a group at Tulane Cancer Center demonstrated that Golgi-targeting compound monensin effectively inhibits EMT-driven cancer cell motility by disrupting the promigratory GOLIM4-TLM1 axis, which is dependent on Golgi pH. Monensin treatment increases the pH within the Golgi lumen, inducing rapid exocytosis of GOLIM4, a promigratory Golgi scaffold protein. This work points to Golgi-associated pathways that may provide new targets and strategies for combating metastatic cancers.
