:: Volume 17, Issue 4 (winter 2017) ::
J Ardabil Univ Med Sci 2017, 17(4): 465-475 Back to browse issues page
Effect of Embelin on Inhibition of Cell Growth and Induction of Apoptosis in k562 Cell Line
Zynab Bargeshadi , Yaghoub Pazhang *
Departement of Biology, Faculty of Sciences, Urmia University, Urmia, Iran , y.pazhang@urmia.ac.ir
Abstract:   (6066 Views)
Background & objectives: Cancer is one of the leading causes of morbidity and mortality worldwide. Leukemia is a cancer of blood cells and bone marrow, which is characterized by abnormal growth of white blood cells, known as blasts. Chronic myeloid leukemia is a clonal hematopoietic stem cell disorder that accounts for 15-20 percent of adult leukemia. Embelin, a natural compound found in the fruit of Embeliaribes plant, has low toxicity and potent anticancer properties. Several studies have shown that the anticancer properties of Embelin are due to inhibition of XIAP (X-linked inhibitor of the apoptosis protein) and modulation of NF-kB signaling pathway. The aim of this study was to investigate the effect of Embelin on the growth and apoptosis of K562 cell line.
Methods: K562 cells were cultured in RPMI-1640 medium containing 10 % FBS and 1% penicillin. Then, the cells were treated with different concentrations of Embelin (2, 4, 6, 8 μM/ml) for 72 hours. MTT assay was used to determine the viability of cells. Hoechst staining and DNA electrophoresis were used for apoptosis analysis.
Result: Based on the results of MTT assay, Embelin inhibited the viability of K562 cells. The results of Hoechst staining showed that DNA fragmentation was increased in the treated cells. DNA electrophoresis analysis revealed that Embelin induced apoptosis.
Discussion: As the results showed, Embelin inhibited the cell growth and induced apoptosis in K562 cells time- and dose-dependently. Therefore, Embelin may be a candidate for treatment of chronic myeloid leukemia.

 
Keywords: K562 Cell Line, Apoptosis, Embelin, Anticancer Effect.
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Type of Study: article | Subject: General
Received: 2017/06/20 | Accepted: 2017/12/21 | Published: 2017/12/31


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