Abstract: Objective: To explore the effect of SP600125, a specific c-jun NH2 terminal protein kinase (JNK) inhibitor, on apoptosis and cell-cycle arrest of the human esophageal cancer cell line Eca-109 induced by 2-(3-carboxy-1-oxopropyl)amino-2-deoxy-D-Glucose （COPADG）and the possible molecular mechanism in COPADG-induced cell apoptosis was discussed. Methods: Eca-109 cells were cultured by using RPMI-1640 and calf serum. Eca-109 cells were pre-incubated with SP600125 for 30min prior to exposure to COPADG at different concentrations and for different time. Changes in expression of P-JNK protein were examined by Western blot；Cell growth inhibitory rate was detected by MTT colorimetric assay；Apoptosis rate and cell-cycle arrest was analyzed by flow cytometry. Results: COPADG could significantly inhibit the proliferation of Eca-109 cells and induce them to apoptosis and cell-cycle arrest in G0/G1 phase. Western blot showed that the protein expression of P-JNK was increased in a dose-dependent manner in Eca-109 cells after stimulated by COPADG. SP600125 remarkablely decreased the protein expression of P-JNK as well as the apoptosis rate and cell growth inhibitory rate in Eca-109 cells induced by COPADG as compared with those treated with only COPADG, meanwhile, cell-cycle arrest in G0/G1 phase progressed to cell-cycle arrest in G2/M phase. .Conclusion: JNK signaling pathway may play an important role in apoptosis of Eca-109 induced by the COPADG.