Abstract: AIM: To investigate the role of c-jun N-terminal kinase (JNK) signaling pathway in the ap-optosis of human chronic myelogenous leukemia cell line K562 induced by arsenic trioxide and the possible mechanisms.METHODS: K562 cells were pre-incu-bated with SP600125 for 3 h prior to exposure to ar-senic trioxide at 4 μmol/L and for different time .The cell morphological changes were observed by inverted phase contrast microscopy .The cell growth inhibitory rate was detected by MTT colorimetric assay .The ap-optosis rate was analyzed by Annexin V/PI fluorescence staining together with flow cytometry .Changes in ex-pression of phospho-JNK protein were examined by ELISA.The mutant P53 expression was assayed by flow cytometry.RESULTS: Arsenic trioxide could significantly inhibit the proliferation of K562 cells and induce their apoptosis.The results of ELISA showed that the protein expression of phospho-JNK was in-creased in K562 cells after stimulated by Arsenic triox-ide.SP600125 remarkablely decreased the protein ex-pression of phospho-JNK as well as the apoptosis rate and the cell growth inhibitory rate, but the mutant P53 expression increased in K562 cells induced by arsenic trioxide as compared with those treated with only ar-senic trioxide.CONCLUSION: JNK signaling path-way may play an important role in the apoptosis of K562 cells induced by arsenic trioxide.

Key words: arsenic trioxide, human chronic my-elogenous leukemia cell line, K562, apoptosis, c-jun terminal kinase