The survival of disseminating tumor cells at the invasive edge and in metastatic foci depends on their ability to counteract anti-tumor immunity. The epithelial–mesenchymal transition (EMT) process is associated with the recruitment of immune-suppressive myeloid cells. The onset of the EMT gene expression program is controlled by several transcriptional master-regulators, including ZEB1. Using engineered breast cancer cell lines with different statuses of ZEB1, we examined the effects of ZEB1 on the expression of different pro-inflammatory cytokines. Our results suggest that ZEB1 plays an important role in regulating the expression of CCL2 (C-C motif ligand 2, a.k.a. MCP-1), the main chemoattractant of monocytes. Forced expression of ZEB1 in epithelial MCF-7 cells significantly increased the expression level of CCL2, which was further enhanced by TNF-α. On the contrary, knock-out of ZEB1 in pseudo-mesenchymal MDA-MB-231 cells led to a complete loss of CCL2 expression. Moreover, this effect was not restored by TNF-α induction. Also, positive ZEB1 status in breast cancer cells promoted the chemoattraction of THP-1 macrophages in co-culture experiments. Analysis of publicly available ChIP-seq data implicated ZEB1 in the regulation of CCL2 gene transcription. Taken together, these data suggest that ZEB1 is involved in the formation of the EMT-associated pro-tumor immune microenvironment.