Abstract: Objective 　To investigate the apoptosis-inducing effect of arsenic trioxide (As₂O₃) on human nasopharyngeal carcinoma and its possible mechanism. Methods 　CNE1 cell line was treated with As₂O₃ at different concent ration. Cell apoptosis was evaluated by flow cytometry, transmission elect ron microscopy and TUNEL methods. The effect of As₂O₃ on the expression of p53, bax and bcl-2 genes was studied with immunohistochemology. Results 　CNE1 cell apoptosis induced by As₂O₃ was detected by FCM, electron microscopy and TUNEL. Typical subdiploid peak before G₀ / G₁ phase was observed by flow cytometric analysis, showing a dose-and time-dependent effect . Morphological feature of apoptosis, including cell shrinkage, nuclear condensation, DNA f ragmentation and formation of apoptotic bodies were found under electron microscopy. After 48h exposure to As₂O₃ at dose of 0. 5mg/ L, 1. 0mg/ L and 2. 0mg/ L apoptosis index (AI) accounted by TUNEL staining were 2. 66 ±0. 64, 8. 15 ±0. 96 and 11. 59 ±0. 68, respectively, which were significantly higher than that of control (0. 43 ±0. 43, P < 0. 05) . The expression of p53, bax protein was increased sharply in CNE1 cell t reated with As₂O₃ . Significant positive correction existed between AI and p53 protein expression ( r = 0. 554, P = 0. 011), AI and bax protein expression ( r = 0. 891, P = 0. 000... ) . There was positive correction between p53 and bax protein expression ( r = 0. 626, P = 0. 003) . Conclusion 　Arsenic trioxide can induce CNE1 cell apoptosis, which was associated with up-regulation of bax and wild-type p53 genes expression.