القای آپوپتوز در رده سلولی HL-60 توسط آرسنیک تری‌اکساید با کاهش نسبت بیان Bcl-2 به Bax در سطح mRNA

Abstractbackground and objectivesarsenic trioxide (as2o3) has been shown to have anti-cancer effects on a wide range of cancers. as2o3 has proved to be the most efficient in treatment of acute promyelocytic leukemia (apl) patients. it primarily acts by triggering apoptosis in cancer cells. to better understand the molecular mechanisms involved in as2o3-induced apoptosis, in the present study we examined the effects of as2o3 both on the expression of bax and bcl-2 (the major regulators of apoptosis), and p53 genes in hl-60 cell line.materials and methodsin this experimental study, the mtt colorimetric assay was used to assess the growth-inhibitory effect of as2o3 on hl-60 cells. the mrna levels of p53, bax and bcl-2 were analyzed by using real-time pcr. data were analyzed by using spss18, t-test and anova tests.resultsas2o3 inhibits the growth of hl-60 cells in a dose dependent manner at 24h. significant decrease (89% ± 3%) in cell viability was observed at 4?m and the ic50 value was about 16 ?m. in hl-60 cell, no expression of p53 was detected. real-time pcr results showed while bax mrna expression was not significantly affected in as2o3 treated hl-60, the bcl-2/bax ratio expression level significantly decreased in a dose dependent manner.conclusionsas2o3 exerts part of its antitumor effect by inducing apoptosis through decreasing bcl-2/bax mrna ratio in p53-null leukemic cell line hl-60. more research on the protein level is required for these results to be reinforced.