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Background and Objective: Lovastatin is a HMG-CoA reductase inhibitor and used for the treatment of hypercholesterolemia. Inhibition of HMG-CoA reductase results in inhibiting the activity of the Ras proto-oncogene that has mutations in most cancers. This study was done to determine the Anti-proliferative and apoptotic effects of Lovastatin on K562 Erthromyloidy cancer cell line.
Methods: The K562 Erthromyloidy cancer cell line were cultured and treated with different concentrations of lovastatin. Their antitumor effect on K562 cells were assessed via MTT assay after 72 hours. Hoechst (33342) staining and DNA electrophoresis were used for study of apoptosis.
Results: Lovastatin had antitumor effect on K562 Erthromyloidy cancer cell line and this effect increased by incease of time and concentration.The maximum inhibitory effect was 59% in higher concentration (100 µM) and 72 hours after the treatment. Reduced cell growth at 24 and 48 hours after treatment was 24% and 43%, respectively. Lovastatin significantly inhibited K562 cell growth (P<0.05).
Conclusion: This study showed that lovastatin has antitumor effect on K562 Erthromyloidy cancer cell line.

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Background and Objective: Chronic myeloid leukemia is one of the most well-known types of leukemia. Inflammation is one of the leading causes of cancer; therefore, anti-inflammatory agents are used for reducing and suppressing the growth of cancer cells. Dexamethasone, a cortisol agonist, has anti-inflammatory, anti-tumor, and apoptotic effects. Diclofenac is a cyclooxygenase enzyme inhibitor with anti-inflammatory properties. This study was performed to determine the synergistic effect of diclofenac and dexamethasone on the growth of K562 cancer cells.
Methods: In this descriptive-analytical study, K562 cell line was cultured in RPMI-1640 medium enriched with glutamine, penicillin, and streptomycin. The cytotoxic effects of dexamethasone, diclofenac and their combination (multi-target tracking) were evaluated using MTT assay. Hoechst staining and DNA electrophoresis were carried out to evaluate the occurrence of apoptosis.
Results: Diclofenac, dexamethasone and their combination had cytotoxic effects on the cells at concentrations of 20, 40, 60, and 80 µmol/ml. A significant cytotoxic effect was observed after 72 hours of treatment with different concentrations of the drugs (P<0.05). Hoechst staining showed that DNA fragmentation was increased in the treated cells. DNA electrophoresis also showed induction of apoptosis by diclofenac, dexamethasone, and their combination.
Conclusion: The combination of diclofenac and dexamethasone at concentration of 20 µmol/ml is more effective in inducing apoptosis in K562 cells compared with each drug alone.