Increased expression of the chemokine CX(3)CL1 and its sole receptor, CX(3)CR1 have been correlated with poor pancreatic cancer patient survival and time to recurrence, as well as with pancreatic perineural invasion. We have previously shown that metastasis of prostate and breast cancer is in part driven by CX(3)CL1, and have developed small molecule inhibitors against the CX(3)CR1 receptor that diminish metastatic burden. Here we ask if inhibition of this chemokine receptor affects the phenotype of PDAC tumor cells. Our findings demonstrate that motility, invasion, and contact-independent growth of PDAC cells all increase following CX(3)CL1 exposure, and that antagonism of CX(3)CR1 by the inhibitor JMS-17-2 reduces each of these phenotypes and correlates with a downregulation of MT phosphorylation. These data suggest that PDAC tumor cell migration and growth, elements critical in metastatic progression, may susceptible to pharmacologic intervention. (C) 2017 The Authors. Published by Elsevier Inc. This is an open access article under the CC BY-NC-ND license.