Study of Bcl-2 siRNA Enhancement of Sensitivity of HL-60 Cells to All Trans Retinoic Acid

来源 :Chinese Journal of Clinical Oncology | 被引量 : 0次 | 上传用户:w15002554773
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OBJECTIVE To study whether siRNA targeting against the Bcl-2 gene can enhance sensitivity of HL-60 cells to all trans retinoic acid(ATRA). METHODS siRNA,which is a leading sequence selected by previous experiments,was transferred into HL-60 cells.At 6 h after transfection,the cells were cultured with ATRA.The cell growth of the HL-60 cells was measured by the MTT assay at 24, 48,72 h.The level of the Bcl-2 protein and ROS(reactive oxygen species)as well as membrane potential of the mitochondria were determined by flowcytometry. RESULTS siRNA significantly increased the inhibitory effect of ATRA on growth of the HL-60 cells.The combination of siRNA with ATRA resulted in a decrease in the Bcl-2 protein level and an increase in the ROS level as well as significantly lowering the mitochondrial membrane potential of the HL-60 cells(P<0.05). CONCLUSION Effective siRNA targeting of Bcl-2 increases the sensitivity of HL-60 leukemic cells to ATRA by inhibiting the expression of the Bcl-2 protein. OBJECTIVE To study whether siRNA targeting against the Bcl-2 gene can enhance sensitivity of HL-60 cells to all trans retinoic acid (ATRA). METHODS siRNA, which is a leading sequence selected by previous experiments, was transferred into HL-60 cells. At 6 h after transfection, the cells were cultured with ATRA. The cell growth of the HL-60 cells was measured by the MTT assay at 24, 48, 72 h. The level of the Bcl-2 protein and ROS (reactive oxygen species RESULTS As siRNA significantly increased the inhibitory effect of ATRA on growth of the HL-60 cells. the combination of siRNA with ATRA resulted in a decrease in the Bcl-2 protein level and an increase in the ROS level as well as significantly decreased the mitochondrial membrane potential of the HL-60 cells (P <0.05). CONCLUSION Effective siRNA targeting of Bcl-2 increases the sensitivity of HL-60 leukemic cells to ATRA by inhibiting the expression of the Bcl-2 protei n.
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