AIM: To investigate 2-methoxyestradiol induced apoptosis and its mechanism of action in CNE2 cell lines. METHODS: CNE2 cells were cultured in RPMI-1640 medium and treated with 2-methoxyestradiol in different concentrations. MTT assay was used to detect growth inhibition. Flow cytometry and DNA ladders were used to detect apoptosis. Western blotting was used to observe the expression of p53, p21WAF1, Bax, and Bcl-2 protein. RESULTS: 2-methoxyestradiol inhibited proliferation of nasopharyngeal carcinoma CNE2 cells with IC50 value of 2.82μmol/L. The results of flow cytometry showed an accumulation of CNE2 cells in G2/M phase in response to 2-methoxyestradiol. Treatment of CNE2 cells with 2-methoxyestradiol resulted in DNA fragmentation. The expression levels of protein p53 and Bcl-2 decreased following 2-methoxyestradiol treatment in CNE2 cells, whereas Bax and p21WAF1 protein expression were unaffected after treatment with 2-methoxyestradiol. CONCLUSION: These results suggest that 2-methoxyestradiol induc AIM: To investigate 2-methoxyestradiol induced apoptosis and its mechanism of action in CNE2 cell lines. METHODS: CNE2 cells were cultured in RPMI- 1640 medium and treated with 2-methoxyestradiol in different concentrations. MTT assay was used to detect growth inhibition. Flow cytometry and DNA ladders were used to detect apoptosis. RESULTS: 2-methoxyestradiol inhibited proliferation of nasopharyngeal carcinoma CNE2 cells with IC50 value of 2.82 μmol / L. The results of flow cytometry showed an accumulation of CNE2 cells in G2 / M phase in response to 2-methoxyestradiol. Treatment of CNE2 cells with 2-methoxyestradiol resulted in DNA fragmentation. The expression levels of protein p53 and Bcl- 2-methoxyestradiol treatment in CNE2 cells, while Bax and p21WAF1 protein expression were unaffected after treatment with 2-methoxyestradiol. CONCLUSION: These results suggest that 2-met hoxyestradiol induc