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자료유형
학술저널
저자정보
저널정보
대한혈액학회 Blood Research Blood Research Vol.50 No.1
발행연도
2015.1
수록면
33 - 39 (7page)

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BackgroundAlthough deferasirox (DFX) is reported to have anti-tumor effects, its anti-leukemic activityremains unclear. We evaluated the effect of DFX treatment on two murine lymphoidleukemia cell lines, and clarified the mechanisms underlying its potential anti-leukemicactivity. MethodsL1210 and A20 murine lymphoid leukemia cell lines were treated with DFX. Cell viabilityand apoptosis were evaluated by the 3-(4,5-dimethylthaizol-2-yl)-5-(3-carboxymethylphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) assay and fluorescence-activated cellsorting (FACS) analysis, respectively. Immunoblotting was performed to detect the expressionof key apoptotic proteins. ResultsIn dose- and time-dependent manner, DFX decreased viability and increased apoptosisof murine leukemic cells. Fas expression was significantly higher in A20 cells than in L1210cells at all DFX concentrations tested. Although both cell lines exhibited high caspase 3and caspase 9 expression, a critical component of the intrinsic mitochondrial apoptoticpathway, expression was greater in L1210 cells. In contrast, caspase 8, a key factor in theextrinsic apoptotic pathway, showed greater expression in A20 cells. Cytochrome c expressionwas significantly higher in L1210 cells. In both cell lines, co-treatment with ferricchloride and DFX diminished the expression of these intracellular proteins, as comparedto DFX treatment alone. ConclusionTreatment with DFX increased caspase-dependent apoptosis in two murine lymphoid leukemiacell lines, with differing apoptotic mechanisms in each cell line.

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