CCL2 recruits inflammatory monocytes to facilitate breast tumor metastasis. This study identifies that Gr1+ inflammatory monocytes (IMs) are preferentially recruited to pulmonary metastases but not primary mammary tumors, a process also observed in human breast cancer. The recruitment of CCR2-expressing IMs and subsequent MAMs is dependent on tumor and stromal-derived CCL2. Inhibition of CCL2/CCR2 signaling using anti-CCL2 antibodies blocks IM recruitment and inhibits metastasis in vivo, prolonging tumor-bearing mice survival. Depletion of tumor-derived CCL2 also inhibits metastatic seeding. IMs promote tumor cell extravasation through monocyte-derived VEGF. CCL2 expression and macrophage infiltration correlate with poor prognosis and metastatic disease in human breast cancer. The study provides a mechanistic link between these clinical associations and indicates new therapeutic targets for treating metastatic breast disease. Monocyte trafficking into primary tumors and metastases was studied using adoptive transfer of mouse or human monocytes in various models. Monocytes and macrophages were recovered by enzymatic disaggregation and FACS analysis. Anti-CCL2 or CCR2 null mutant mice were used to test mechanisms behind monocyte recruitment. VEGF expression in monocytes was ablated using a tamoxifen-inducible Cre strain. Effects of monocyte depletion on tumor cell extravasation were determined using an ex vivo lung imaging system and in vitro extravasation assays. CCL2 synthesized by metastatic tumor cells and target site stroma is critical for recruiting CCR2-expressing monocytes that enhance tumor cell extravasation. Mechanistically, this is at least in part through targeted delivery of molecules like VEGF that promote extravasation. IMs are continuously recruited by CCL2 and differentiate into macrophages that promote metastatic growth. These findings suggest that targeting monocyte recruitment and function could be a therapeutic approach for metastatic breast disease.CCL2 recruits inflammatory monocytes to facilitate breast tumor metastasis. This study identifies that Gr1+ inflammatory monocytes (IMs) are preferentially recruited to pulmonary metastases but not primary mammary tumors, a process also observed in human breast cancer. The recruitment of CCR2-expressing IMs and subsequent MAMs is dependent on tumor and stromal-derived CCL2. Inhibition of CCL2/CCR2 signaling using anti-CCL2 antibodies blocks IM recruitment and inhibits metastasis in vivo, prolonging tumor-bearing mice survival. Depletion of tumor-derived CCL2 also inhibits metastatic seeding. IMs promote tumor cell extravasation through monocyte-derived VEGF. CCL2 expression and macrophage infiltration correlate with poor prognosis and metastatic disease in human breast cancer. The study provides a mechanistic link between these clinical associations and indicates new therapeutic targets for treating metastatic breast disease. Monocyte trafficking into primary tumors and metastases was studied using adoptive transfer of mouse or human monocytes in various models. Monocytes and macrophages were recovered by enzymatic disaggregation and FACS analysis. Anti-CCL2 or CCR2 null mutant mice were used to test mechanisms behind monocyte recruitment. VEGF expression in monocytes was ablated using a tamoxifen-inducible Cre strain. Effects of monocyte depletion on tumor cell extravasation were determined using an ex vivo lung imaging system and in vitro extravasation assays. CCL2 synthesized by metastatic tumor cells and target site stroma is critical for recruiting CCR2-expressing monocytes that enhance tumor cell extravasation. Mechanistically, this is at least in part through targeted delivery of molecules like VEGF that promote extravasation. IMs are continuously recruited by CCL2 and differentiate into macrophages that promote metastatic growth. These findings suggest that targeting monocyte recruitment and function could be a therapeutic approach for metastatic breast disease.