Idiopathic pulmonary fibrosis (IPF) is the most common interstitial lung disease. However, the pathogenesis remains to be fully elucidated. Melatonin is secreted by the pineal gland, it has a strong antioxidant effect, and exerts an anti-fibrosis effect. Whether melatonin attenuates pulmonary fibrosis by inhibiting epithelial-mesenchymal transition (EMT) requires further research. The present study aimed to investigate whether melatonin prevents transforming growth factor-beta 1 (TGF-beta 1)-induced EMT and underlying signaling pathways using reverse transcription-quantitative polymerase chain reaction, western blot analysis and immunofluorescence. The results demonstrated that melatonin inhibits EMT in A549 cells, and the Wnt/beta-catenin and Smad2/3 signaling pathways are involved in the EMT of the A549 cell line as they were suppressed by melatonin. The present study indicates that melatonin inhibited TGF beta 1-induced epithelial-mesenchymal transition in the A549 cell line and may potentially be useful in the treatment of IPF.