Objective To investigate whether miR-200c can alleviate fibrosis in renal tubular epithelial cells induced by transforming growth factor-β1 (TGF-β1-induced) via the regulation of autophagy. Methods HK2 cells were stimulated with TGF-β1 at different concentrations (0,5, 10,15, 20,30ng/ml) for 48h, the cell morphology was observed under an inverted microscope, and the cell proliferation was detected by CCK-8. The concentration (c) of TGF-β1, which induced the most rapid proliferation of HK2 cells, was selected for transfection. The cells were transfected with 40nmol/L nonsense RNA (NC group), being treated with 40nmol/L nonsense RNA (NC+T group) for 48 h, with 40 nmol/L miR-200c mimics (M group), and with 40nmol/L miR-200c mimics (M+T group). qRT-PCR was used to detect the transfection efficiency of mir-200c. Western blotting was used to detect the expression of Smad pathway protein Smad2 and Smad3, α-smooth muscle actin(α-SMA), E-cadherin (E-cad), autophagy-related protein LC3 and p62. Results HK2 cells stimulated by TGF-β1 at 10ng/ml proliferated the fastest 48h later. Microscopic morphology of HK2 cells changed from normal oval paving stone to long fusiform with the most obvious fibrosis. qRT-PCR showed that the expression of miR-200c in group M was(212.42±12.25) times higher than that in group NC (t=24.41, P=0.000), indicating that the transfection was effective. Western blotting showed that expression of Smad2, Smad3 and α-SMA in HK2 cells in NC+T group increased and E-cad protein expression decreased compared with NC group (P<0.05). Compared with NC+T group, the expression of Smad2, Smad3 and α-SMA in M+T group decreased, and the expression of E-cad increased (P<0.05), suggesting that the increase of miR-200c expression inhibited fibrosis. It was further found that the expression of LC3-Ⅱ/LC3-Ⅰin M group was higher than that in NC group, and the expression of p62 was lower, suggesting increased autophagy; the expression of LC3-Ⅱ/LC3-Ⅰ in M+T group was higher than that in NC+T group, and the expression of p62 was lower, suggesting that the increased expression of miR-200c alleviated fibrosis. Conclusion miR-200c may alleviate TGF-β1-induced renal tubular epithelial fibrosis by activating autophagy.