The movement of cancer cells out of their primary organ of origin greatly reduces the chances of cure (Wells et al., 2013; herein incorporated by reference in its entirety). Increased cell motility is a quintessential characteristic of the metastatic phenotype, represents an initial step in the metastatic cascade, and is absolutely necessary for cancer cells to move from their primary organ of origin to a distant metastatic site (Talmadge and Fidler, 2010; herein incorporated by reference in its entirety). The development of distant metastases is a primary cause of the majority of cancer-associated morbidity and mortality (Minn and Massague, 2008; herein incorporated by reference in its entirety). Processes that drive the development of increased cell motility and metastasis have high potential value as therapeutic targets. However, comprehensive endeavors aimed at selectively inhibiting cancer cell motility and resultant metastasis have met with failure (Coussens et al., 2002; Krishna and Bergan, 2014; Steeg, 2006; herein incorporated by reference in their entireties). While many pathways have been shown to regulate cell motility and metastasis, they constitute pathways whose regulatory effects are pleiotropic (Krishna and Bergan, 2014; herein incorporated by reference in its entirety). It has therefore not been possible to identify regulators of cell motility and metastasis that possess enough selectivity to support their targeted manipulation.