ABSTRACT Diverse RNA transcripts acting as competing endogenous RNAs (ceRNAs) can co-regulate each other's expression by competing for shared microRNAs. CCR2 protein, the receptor for CCL2, is implicated in cancer progression. However, we found that a higher CCR2 mRNA level is remarkably associated with prolonged survival of breast cancer patients. These conflicting results prompted us to study the non-coding function of CCR2 mRNA. We found that the CCR2 3′ untranslated region (UTR) inhibited MDA-MB-231 and MCF-7 cell metastasis by repressing epithelial–mesenchymal transition (EMT) in vitro, and suppressed breast cancer metastasis in vivo. Mechanistically, the CCR2 3′UTR modulated the expression of the RhoGAP protein STARD13 via acting as a STARD13 ceRNA in a microRNA-dependent and protein coding-independent manner. The CCR2 3′UTR blocked the activation of RhoA–ROCK1 pathway, which is the downstream effector of STARD13, and thus decreased the phosphorylation level of myosin light chain 2 (MLC2) and formation of F-actin. Additionally, the function of the CCR2 3′UTR was dependent on STARD13 expression. In conclusion, our results confirmed that the CCR2 3′UTR acts as a metastasis suppressor by acting as a ceRNA for STARD13 and thus inhibiting RhoA–ROCK1–MLC–F-actin pathway in breast cancer cells. This article has an associated First Person interview with the first author of the paper.