Intracellular calcium influx mediates invasiveness of colon cancer cell via destabilization of focal adhesion kinase

Carcinogenic induction in a colon occurs through a sequence of events leading to metastasis that involved various oncogenic proteins. Focal adhesion kinase (FAK) regulates metastatic adhesion of carcinoma cells, and it has recognized as a potential therapeutic target to metastatic colon cancer. However, calcium (Ca 2+ ) dependent calpain-FAK pathway to clear up the mechanism of motility has not been understood. Recently, Ca 2+ bound lactate was used to induce intracellular Ca 2+ (iCa 2+ )influx into colorectal cancer (CRC) cells, and we confirmed that iCa 2+ influx mediated FAK destabilization and CRC cell motility. Calpeptin, a calpain inhibitor, restored the effect of iCa 2+ influx on the CRC cells. We herein discuss the phenomenon of an increase in the CRC cell motility that focused on the iCa 2+ influx-induced FAK cleavage via calpain.