[Cytotoxic effects of selective inhibitor 'Aurora Kinase B' on viability and metabolic features of human promyelocytic leukemia cell line]

A goal of modern cancer research is to reach targeted therapies with drugs having fewer side effects. AZD1152 is a highly specific inhibitor of Aurora Kinase B, which leads to the programmed cell death by different mechanisms. The aim of this study was to evaluate the effects of AZD1152 on viability and metabolic activity of NB4 cells [APL derived cell line]. The cells were treated with various concentrations of AZD1152. After 24, 48 and 72h treatments, the metabolic activity and viability of inhibitor-treated NB4 cells were assessed using MTT and trypan blue dye exclusion assays, respectively. Data were analyzed by applying student's t-test [Microsoft Excel]. At 25, 50 and 100 nM, AZD1152 reduced the metabolic activity by 9.2, 15.5 and 56.2% [after 24h], 10.3, 19.5 and 59.9% [after 48h], and 17.1, 28.4 and 64.8% [after 72h], respectively. Meanwhile, the percentage of viability was decreased to about 51, 45 and 40% [after 24h], 39, 36 and 30% [after 48h], and 34, 32 and 28% [after 72h], respectively. According to the results, AZD1152 has substantial efficacy on APL cell line and may be applied in some cases, e. g., for patients who have relapse or who become refractory to the conventional chemotherapy. Further studies are needed to show the molecular mechanisms regulating effects of this anti-cancer agent

[Assesment of the efficacy of hesa-a on the proliferation and apoptosis of chronic myelogenous leukemia cell line [K562]]

Chronic myelogenous leukemia is characterized by Philadelphia [Ph] chromosome, the presence of BCR-ABL fusion gene and constitutive activation of the ABL1 tyrosine kinase. Despite an excellent result of target therapy by imatinib, some patients develop resistance to imatinib. In this study Efficacy of HESA-A on proliferation and apoptosis of K562 cell line was assessed. In this study doubling time of K562 cell line was calculated. The cells were affected by various concentrations of HESA-A[1,2,4 and 8 mg/ml respectively]. Cytotoxicity and IC50 dose of HESA-A were detected by MTT and trypan blue exclusion assay. Apoptosis was assessed by flowcytometry after 48 h cell treatment in the presence of IC50 dose. Doubling time of K562 cells was 24 hours. HESA-A reduced the number of viable K562 cells in a concentration dependent manner.IC50 dose was 3.5 mg/ml. In flowcytometry analysis of apoptosis, 19.22% of the treated cells were located in the position of the necrotic cells. The results of MTT and trypan blue exclusion assay suggest that HESA-A inhibits the growth of k562 cells in a concentration dependent manner and induces necrosis in K562 cells