Abstract
Human SIRT1 is an enzyme that deacetylates the p53 tumor suppressor protein. It has been suggested to modulate p53-dependent functions including DNA damage-induced cell death. Sirtuins are nicotinamide adenine dinucleotide dependent class III histone deacetylase proteins that play a crucial role in several cellular processes, including DNA repair, apoptosis, and lifespan. In this study, we investigated the relationship between sirtinols and apoptosis mechanism at leukemic cells. For this, we applied sirtinol to K-562 (chronic myeloid leukemia) and Jurkat (acute T-cell leukemia) cell lines at different dilutions in cell culture conditions. And Cdna isolated patient RNA samples, after that Caspase3, Bax, Bcl2 expression performed with used qRT-PCR technique and cells were stained by Annexin V method. According to the results of research, we identified that Sirtinol dilutions were increased in both K-562 and Jurkat, while the number of living cells was decreasing, the number of dead cells increased at 50 μM dilution. Sirtinol, an HDAC inhibitor in the direction of these results, has been observed to be a drug that can be effective in the treatment of CML as well as T-ALL.
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