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Gambogic acid induces mitochondria-dependent apoptosis by modulation of Bcl-2 and Bax in mantle cell lymphoma JeKo-1 cells
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2013
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MitophagyApoptosisImmunologyBlood CellCell DeathCell Death MechanismsCellular PhysiologyTumor BiologyOxidative StressInflammationHematological MalignancyMantle CellAutophagyGambogic AcidCell SignalingMitochondrial Membrane PotentialJeko-1 CellsCell BiologyMitochondrial FunctionMalignant Blood DisorderMedicine
Aim: To study the mechanisms in gambogic acid (GA) -induced JeKo-1 human Mantle Cell Lymphoma cell apoptosis in vitro. Methods: The proliferation of GA-treated JeKo-1 cells was measured by CCK-8 assay and Ki-67 immunocytochemical detection. Apoptosis, cell cycle and mitochondrial membrane potential were measured by flow cytometric analysis. Caspase-3,-8 and -9 were detected by colorimetric assay. Bcl-2 and Bax were analyzed by Western blotting. Results: GA inhibited cell growth in a time-and dose-dependent manner. GA induces apoptosis in JeKo-1 cells but not in normal bone marrow cells, which was involved in reducing the membrane potential of mitochondria, activating caspases-3, -8 and -9 and decreasing the ratio of Bcl-2 and Bax without cell cycle arresting. Conclusions: GA induced apoptosis in human MCL JeKo-1 cells by regulating Bcl-2/Bax and activating caspase-3, -8 and -9 via mitochondrial pathway without affecting cell cycle.