Tehran University of Medical Sciences International Journal of Hematology-Oncology and Stem Cell Research 2008-2207 6 1 2012 03 15 30 35 Shahrbano Rostami Tarbiat Modares University, Tehran, Iran Saeid Abroun Tarbiat Modares University, Tehran, Iran Kamran Alimoghaddam Hematology-Oncology and Stem Cell Transplantation Research Center, Tehran, Iran Mehrdad Nourozinia Tarbiat Modares University, Tehran, Iran Bahram Chahardouli Department of Hematology, School of Allied Medical Sciences, Tehran University of Medical Sciences, Tehran, Iran Ardeshir Ghavamzade Hematology-Oncology and Stem Cell Transplantation Research Center, Tehran, Iran 2015 10 01 Introduction: Arsenic Trioxide (As2O3) causes antitumor effects by various mechanisms, including degradation of PML-RARA in the acute promyelocytic cells, growth inhibition and induction of apoptosis. However, the precise mechanisms of these processes remain incompletely understood. The purpose of this study was to evaluate the effects of arsenic trioxide on cell growth, cell cycle regulation and apoptosis in PML/RARA negative acute promyelocytic leukemia cell line HL-60. Methods: The cytotoxic effect of As2O3 was assessed by MTT assay, Apoptosis was detected by flow cytometry analysis using annexin V–FITC/PI and cell cycle distribution was evaluated by propidium iodide staining. Results: MTT assay showed that cell growth was inhibited in a time- and dose-dependent manner. As2O3 exerts growth inhibitory effect by arresting the cells at G2/M phase. Apoptosis analysis revealed that As2O3 treatment induced apoptosis at the lower concentrations, while necrosis occurred at the higher concentrations. Conclusion: As2O3 inhibits growth and induces apoptosis of HL-60 cells through induction of cell cycle arrest. Further studies are required to elucidate the molecular mechanisms of As2O3-induced anti-tumor effects. https://ijhoscr.tums.ac.ir/index.php/ijhoscr/article/view/324 https://ijhoscr.tums.ac.ir/index.php/ijhoscr/article/download/324/310