Arsenic trioxide-induced apoptosis in HL-60 cell line by decreasing the ratio of Bcl-2 to Bax mRNA expression. (English)

Background and Objectives Arsenic trioxide (As 2 O 3 ) has been shown to have anti-cancer effects on a wide range of cancers. As 2 O 3 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 As 2 O 3 -induced apoptosis, in the present study we examined the effects of As 2 O 3 both on the expression of Bax and Bcl-2 (the major regulators of apoptosis), and p53 genes in HL-60 cell line. Materials and Methods In this experimental study, the MIT colorimetric assay was used to assess the growth- inhibitory effect of As 2 O 3 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 SPSSI8, t-test and ANOVA tests. Results As 2 O 3 inhibits the growth of HL-60 cells in a dose dependent manner at 24h. Significant decrease (89% ± 3%) in cell viability was observed at 4MM and the 1C50 value was about 16 MM. In HL-60 cell, no expression of p53 was detected. Real-time PCR results showed while Bax mRNA expression was not significantly affected in As 2 O 3 treated HL-60, the Bcl-2IBax ratio expression level significantly decreased in a dose dependent manner. Conclusions As 2 O 3 exerts part of its antitumor effect by inducing apoptosis through decreasing BcI-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. [ABSTRACT FROM AUTHOR]

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