While the importance of cancer stem cells is gaining ground in the cancer field, little is known about the signaling molecules that drive the cancer stem cell phenotype. The role of cancer stem cells in promoting metastasis is another area that is just beginning to be explored. We asked whether RhoC GTPase, a known metastatic oncogene, is involved in promoting the aggressive nature of ALDH+ breast cancer stem cells. We transfected the normal-like mammary epithelial cell line MCF-10A with either a control plasmid (10A vec) or a plasmid for constitutively active RhoC (10A G14V). We also transfected the RhoC-overexpressing inflammatory breast cancer (IBC) cell line SUM149 with either scrambled control (149 scr) or shRNA targeting RhoC (149 shRhoC). The transfected cells were sorted for ALDH activity and the corresponding ALDH+/- populations were orthotopically xenografted into the mammary fat pads of NOD/SCID mice. Overexpressing RhoC G14V in MCF-10A cells caused the cells to form prominent lung metastases without forming a primary tumor. Accordingly, inhibiting RhoC in SUM149 cells significantly decreased the number of mice presenting with lung metastases. Interestingly, the metastatic potential of the ALDH+ cell populations was similarly affected by altered RhoC expression: ALDH+ 10A vec and 149 shRhoC cells formed significantly fewer metastases than their RhoC-overexpressing counterparts. From these findings we conclude that RhoC is a potent driver of lung metastasis in breast cancer - independent of primary tumor formation - and is capable of modulating the metastatic potential of breast cancer stem cells.