Background and Aims: Naringin (NAR) is a natural flavonoid compound, which can inhibit the growth of cells of cervical cancer, gastric cancer, tongue squamous cell carcinoma and liver cancer, but its effect on thyroid cancer cells is not clear. Therefore, this study was conducted to investigate the effects of NAR on thyroid cells, and to preliminarily analyze its mechanism, so as to provide a theoretical basis for research and development of drugs against thyroid cancer.  
Methods: Thyroid cancer ACT-1 cells were cultured with different concentrations of NAR for different time periods, and then, the cell viability rates were determined by MTT assay to observe the time and concentration effects of NAR on ACT-1 cells, and calculate the IC50 values. Based on above experiment, the proper concentrations of NAR and proper time span were chosen to treat the ACT-1 cells. After that, the cell apoptosis was detected by Annexin V-FITC/PI staining, change in autophagic bodies was observed by green fluorescent protein (GFP)-labeled plasmid transfection, and the changes in expressions of the autophagy-associated proteins (LC3 I, LC3 II, p62) and proteins in the AMPK/mTORC1 pathway, as well as the influences of AMPK inhibitor on NAR actions were examined by Western blot analysis. 
Results: The survival of ACT-1 cells was significantly suppressed in a time- and concentration dependent manner by NAR treatment (all P<0.05), and the IC50 values for 12, 24 and 48 h were 85.65, 50.12 and 38.94 μg/mL, respectively. In ACT-1 cells after treatment with the selected concentrations of 25, 50 and 100 μg/mL NAR, the apoptosis rates, numbers of autophagic bodies and the protein expression levels of LC3 II/LC3 I and p-AMPK/AMPK were significantly increased, and the protein expression levels of p62 and p-mTORC1/mTORC1 were significantly decreased, with a concentration-dependent manner (all P<0.05). In ACT-1 cells after treatment with 100 μg/mL NAR and simultaneous 25 μmol/L AMPK inhibitor, the above effects as well as the apoptosis-functional protein caspase-3 increasing effect of NAR on ACT-1 cells were all significantly suppressed (all P<0.05). 
Conclusion: NAR can inhibit the proliferation and induce the apoptosis in thyroid cancer ACT-1 cells, which may be related to its regulating AMPK/mTORC1 signaling pathway and the enhancing autophagy.