Objective To investigate the effects of mitochondrial ferritin (FtMt) on epithelial mesenchymal transition (EMT) of-cisplatin-resistant non-small lung cancer line A549 / DDP and non-small lung cancer line A549, and to explore the molecular mechanism in improving cisplatin resistance. Methods Flow cytometry was used to determine the apoptosis rate and cell cycle of A549 and A549 / DDP cells. Western blot was used to analyze expression of E-cadherin, N- cadherin and FtMt. RT-qPCR was used to measure gene expression of E-cadherin, N-cadherin, snail, slug, twist, vimentin, FPn, DMT1, hepcidin and TfR1 in cells. Cell migration was assessed by a scratch assay. Results The apoptotic rate of A549 / DDP and A549 cells was increased with the increase in cisplatin concentration, and the apoptotic rate of A549 cells was significantly higher than that of A549 / DDP cells. After cisplatin treatment, A549 cells in G0 / G1 and G2 / M phases were gradually decreased in all groups compared with the 0 μg / mL cisplatin group, whereas A549 / DDP cells in G0 / G1 and G2 / M phases were first increased and then decreased (P<0. 05). The protein and mRNA levels of E-cadherin in A549 / DDP cells were lower than those in A549 cells, while the protein and mRNA levels of N-cadherin in A549 / DDP cells were higher than those in A549 cells. The mRNA levels of snail, slug, vimentin, FPn, hepcidin and TfR1 in A549 / DDP cells were higher than those in A549 cells (P<0. 05). The mRNA level of DMT1 in A549 / DDP cells was lower than that in A549 cells (P>0. 05). The cell migration rate was significantly faster in A549 / DDP cells than in A549 cells (P<0. 05). The expression of FtMt in A549 / DDP cells was significantly higher than that in A549 cells (P< 0. 05). Conclusions Cisplatin resistance of lung cancer cells is related to the EMT process, and FtMt might play an important role in cisplatin resistance of lung cancer cells.