Using in vitro model systems of Ishikawa endometrial epithelial cells stably expressing the FP receptor to levels seen in endometrial cancer (FPS cells) and human umbilical vein endothelial cells (HUVECs), we found that ADAMTS1 was regulated in epithelial cells via the PGF2α-FP receptor mediated activation of the calmodulin-NFAT pathway increasing epithelial cell invasion and negatively controlling endothelial cell proliferation. The gene discussed is ADAMTS1; the disease is endometrial cancer.