Deguelin blocks cells survival signal pathways and induces apoptosis of HL-60 cells in vitro

作者：Chen Yan; Wu Qing; Cui Guo hui; Chen Yi quan; Li Rui

来源：International Journal of Hematology, 2009, 89(5): 618-623.

DOI：10.1007/s12185-009-0307-4

• Deguelin
• HL-60 cell
• Survivin
• Bcl-2
• p-AKT

To investigate the anti-cancer effects and molecular mechanism of deguelin on the human leukemia HL-60 cells, to explore the expression and clinical significance of p-AKT, survivin and Bcl-2 in leukemia cell line HL-60 cell. Cell growth rate was assessed by MTT assay. Apoptotic index was evaluated by TUNEL staining. Apoptosis was detected by Annexin V-FITC Apoptosis Detection Kit and transmission electron microscopy (TEM), expression of p-Akt, Bcl-2 and surviving in HL-60 cells was checked by Western blot. Deguelin presented striking proliferation inhibition potency on HL-60 cells in vitro, with the I(C50) value for 48 h being 20.14 nM, and induced apoptosis in HL-60 in a concentration-time-dependent manner. Apoptotic bodies and cell shrinkage and fragmentation were observed by TUNEL and TEM. Deguelin-induced cells morphological changes and degraded several kinase proteins, including Bcl-2 and survivin (members of lap). The degradation of these kinases blocked PI3K/Akt survival signal pathways, inducing apoptosis. Deguelin may induce HL-60 cell apoptosis through depletion of multiple kinase proteins and blockage of survival signal pathways of HL-60 cells.

• 出版日期2009-6
• 单位华中科技大学