Epithelial-to-mesenchymal transition (EMT) is believed to play key roles in the process of cancer metastasis. The molecular changes during EMT are characterized by the down-regulation of epithelial proteins, such as E-cadherin, and the up-regulation of mesenchymal proteins, such as vimentin (VIM). It has been demonstrated that l-kynurenine (l-Kyn), a physiological ligand of Aryl hydrocarbon receptor (Ahr), promotes cancer cells to metastasize. However, the effects of d-enantiomer of kynurenine, d-kynurenine (d-Kyn), on metastasis are still unclear. In the present paper, we firstly confirmed that d-Kyn (10, 40, 60, and 100 µM) positively regulated the metastasis of 95D cells, a lung cancer cell line, which was reduced upon siRNA_Ahr treatment. Moreover, significant enhancement VIM expression was detected in the presence of d-Kyn (10 and 40 µM). In contrast, 10 µM d-Kyn markedly attenuated E-cadherin level. Additionally, 10 µM d-Kyn-mediated changes of VIM and E-cadherin were substantially attenuated on siRNA_Ahr treatment as well. Most importantly, the evidences—10/40 µM d-Kyn-induced up-regulation of CYP1A1, 10 µM d-Kyn-induced increase of nuclear transfer of Ahr, and 10/40/60/100 µM d-Kyn-induced enhancement of DER-luciferase activity—indicated that d-Kyn was capable of activating Ahr in fact. These results suggest that d-Kyn increases lung cancer cells to metastasize by activating Ahr.