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The Effect of Prednisolone on Mir 15A and Mir16-1 Expression Levels and Apoptosis in Acute Lymphoblastic Leukemia Cell Line: Ccrf-Cem Publisher Pubmed



Azimi A1 ; Hagh MF2 ; Yousefi B3 ; Rahnama MA4, 5 ; Khorrami A1 ; Heydarabad MZ2 ; Najafpour M6 ; Hallajzadeh J1 ; Ghahremani A1
Authors
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Authors Affiliations
  1. 1. Maragheh University of Medical Sciences, Department of Basic Sciences, Majles sq. Tehran St., Maragheh, 5156954696, Iran
  2. 2. Hematology and Oncology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
  3. 3. Department of Biochemistry, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran
  4. 4. Department of Hematology, Faculty of Medical Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
  5. 5. School of Advanced Technologies in Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran
  6. 6. Medical Biotechnology Research Center, Guilan University of Medical Sciences, Rasht, Iran

Source: Drug Research Published:2016


Abstract

Background: Glucocorticoids are probably the most important drugs in the treatment of childhood acute lymphoblastic leukemia (ALL). Prednisolone exerts its effect by induce apoptosis in lymphoid lineage cells. Micro RNAs are 18-24 nucleotides RNA implicated in the control of essential biological functions, including apoptosis. In the following study, the effect of prednisolone on the expression of miR 15a & miR16-1 and apoptosis in the CCRF-CEM cell line is investigated. Methods: The cell line of CCRF-CEM was cultured in standard conditions. The changes in the miR 15a and miR 16-1 expression levels were determined by Real Time-PCR technique. Also, the apoptosis is evaluated by flow cytometry using Annexin V and PI staining. Results: This study revealed that, the prednisolone induced apoptosis in a time dependent manner. Prednisolone in concentration of 700 μM was significantly increased the expression of miR 16-1 and miR 15a after 24 h and 48 h treatment (p<0.05). Conclusion: prednisolone-induced apoptosis might be mediated by up-regulation of these 2 miRNAs in CCRF-CEM cells. © Georg Thieme Verlag KG Stuttgart, New York.
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