Background: Studies showed that miR-532-5p suppresses proliferation and induces apoptosis of lung cancer (LC) cells; its role in LC is not fully understood. Therefore, this research aimed to reveal the effect and mechanism of miR-532-5p on migration and invasion of LC cells. Materials and Methods: The transfection efficiencies of miR-532-5p mimic, inhibitor, and overexpressed CCR4 were measured by quantitative real-time polymerase chain reaction (qRT-PCR). The relationships between miR-532-5p and CCR4 in A549 and SBC-5 cells were predicted by targetScan and verified by dual-luciferase reporter assay, Western blot, and qRT-PCR. Migration and invasion of cells transfected with miR-532-5p mimic, inhibitor, and CCR4 were determined by scratch test and transwell assay, respectively. The levels of epithelial-to-mesenchymal transition (EMT)-related proteins (E-cadherin (E-Cad)), N-catenin (N-Cad), and vimentin) in cells were measured by Western blot. Results: MiR-532-5p mimic suppressed migration and invasion, while miR-532-5p inhibitor promoted migration and invasion of cells. CCR4 was a downstream target of miR-532-5p and both its protein and mRNA expressions were inhibited by miR-532-5p mimic, but promoted by miR-532-5p inhibitor. CCR4 promoted migration, invasion, and EMT process, and such effects of CCR4 were reversed by miR-532-5p mimic. Conclusion: MiR-532-5p functioned as a cancer suppressor by negatively regulating CCR4 in LC cells, pointing to a potential protective mechanism of miR-532-5p to LC patients.