Zhongguo shi yan xue ye xue za zhi · 2016
[Action Mechanism of Chlorambucil against Mantle Cell Lymphoma Cell Line Jeko-1].
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Guo Jian-Xin, Zhou Ya-Hong, Pan Jing-Xin, Guo Xi-Zhe, Wu Shi-Xin, Huang Yue-Qin
Аннотация
OBJECTIVE: To explore the action mechanism of chlorambucil against mantle cell lymphoma cell line Jeko-1.
METHODS: The effect of chlorambucil on Jeko-1 cell proliferation was measured by MTT method. The effect of chlorambucil on the apoptosis of Jeko-1 cell was detected by Hoechst staining and Annexin V-FITC dual staining. The activation of PI3K/AKT signaling pathway and the expression of BAX, BCL-2, procaspase 3, procaspase 8 and procaspase 9 were detected by Western blot.
RESULTS: 0, 5, 10, 20 µmol/L chlorambucil could inhibit Jeko-1 cell proliferation at 24, 48, 72 h in a time- and dose-dependent manner. Chlorambucil of 0, 5, 10, 20 µmol/L increased the apoptotic rate of Jeko-1 cells, upregulated the expression of BAX, procaspase 3, procaspase 8, procaspase 9 and PI3K, increased the phosphorylation of AKT and down-regulated the expression of BCL-2.
CONCLUSION: The chlorambucil can induce the apoptosis of mantle cell lymphoma Jeko-1 cells via blocking PI3K/AKT signaling pathway.
METHODS: The effect of chlorambucil on Jeko-1 cell proliferation was measured by MTT method. The effect of chlorambucil on the apoptosis of Jeko-1 cell was detected by Hoechst staining and Annexin V-FITC dual staining. The activation of PI3K/AKT signaling pathway and the expression of BAX, BCL-2, procaspase 3, procaspase 8 and procaspase 9 were detected by Western blot.
RESULTS: 0, 5, 10, 20 µmol/L chlorambucil could inhibit Jeko-1 cell proliferation at 24, 48, 72 h in a time- and dose-dependent manner. Chlorambucil of 0, 5, 10, 20 µmol/L increased the apoptotic rate of Jeko-1 cells, upregulated the expression of BAX, procaspase 3, procaspase 8, procaspase 9 and PI3K, increased the phosphorylation of AKT and down-regulated the expression of BCL-2.
CONCLUSION: The chlorambucil can induce the apoptosis of mantle cell lymphoma Jeko-1 cells via blocking PI3K/AKT signaling pathway.