Objective To explore the anti-tumor effects of anlotinib, a small molecular tyrosine kinase inhibitor, on nasopharyngeal carcinoma (NPC) cells and its potential mechanism, and to provide reliable experimental evidence for the clinical treatment of NPC with anlotinib.Methods The responses of serial dose gradients of anlotinib on the cell viability and proliferation of 6-10B and SUNE-1 cell lines were detected by cell proliferation viability assay and colony formation assay. Then, the downstream pathway proteins in cell lines after anlotinib treatment were visualized by Western blotting. The effects of promoting apoptosis and inducing cell cycle arrest by anlotinib were confirmed through flow cytometry. The capacity of anlotinib in inhibiting migration and invasion of 6-10B and SUNE-1 cell lines was verified by transwell assay and wound healing assay.Results After treatment of anlotinib, cell viability and proliferation were inhibited in nasopharyngeal carcinoma 6-10B and SUNE-1 cell lines in a dose-dependent way, and the inhibition rate was up to 50% when then concentration of anlotinib was 2 μmol·L^-1 (P<0.01). Western blotting results showed that anlotinib might induce the cell apoptosis by activating the mitochondrial pathway and potentially the Erk pathway, with the highest apoptosis rate when the anlotinib concentration up to 2 μmol·L^-1. The results of flow cytometry showed that 2 μmol·L^-1 anlotinib induced remarkable cell apoptosis, with early apoptosis predominantly (P<0.001). What's more, the nasopharyngeal carcinoma cells had obvious changes in cycle distribution after treated with 2 μmol·L^-1 anlotinib. Both 6-10B and SUNE-1 cells had a G₂/M arrest, and there was a significant difference in 6-10B group (P=0.0004), but no statistical differences in SUNE-1 group (P=0.0723). By transwell assay and wound healing assay, the significant suppression of invasion and migration in 6-10B and SUNE-1 was definitude (P<0.05).Conclusion This study indicated that anlotinib promoted the apoptosis and inhibited the proliferation of nasopharyngeal carcinoma cells 6-10B and SUNE-1 through the Erk pathway. It could be a potential target drug for nasopharyngeal carcinoma.