Pancreatic cancer is the 5th leading cause of death among various cancers and is characterized by poor prognosis. Recently, pancreatic stellate cells (PSCs) have been identified as one of the causes to increase the malignancy of pancreatic cancer. In this study, we focused on transient receptor potential melastatin 7 (TRPM7) channel. TRPM7 is ubiquitously expressed in various tissues and cells and reported to be involved in cell proliferation ability, gene expression, and differentiation.
　To investigate the function of TRPM7 in PSCs, we constructed TRPM7 conditional knock out (cKO) mouse using the Tamoxifen (Tam)-inducible Cre / loxP system. The expression of TRPM7 was confirmed both in vivo and in vitro, which was abolished by Tam administration. We investigated the condition of Tam administration to PSCs isolated from TRPM7 cKO mouse and found that it takes one week for TRPM7 to be completely down-regulated after Tam induction.
　PSCs activate the surrounding pancreatic cancer cells by inflammatory cytokines and growth factors such as Platelet-Derived Growth Factor (PDGF). When PSCs were treated with PDGF, enhanced expression of TRPM7 was confirmed.
　In conclusion, our data suggest that TRPM7 is very stable in PSC and is involved in the activation of PSCs.