Wortmannin induced apoptosis of leukemia cells by reducing PI3K/Akt

• Published in: The Chinese-German journal of clinical oncology Vol. 9; no. 12; pp. 734 - 738
• Main Authors: Wang, Xiaonan, Wu, Qing, Zhang, Liansheng, Wu, Yiping, Shu, Yanwen
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer-Verlag 01.12.2010
• Subjects: Cancer Research; DNA链断裂; K562细胞; Medicine; Medicine & Public Health; Oncology; Surgical Oncology; 单细胞凝胶电泳; 浓度依赖性; 渥曼青霉素; 白血病; 细胞凋亡; 细胞增殖; p-AKT; K562 cell; Wortmannin; NF-KB
• ISSN: 1610-1979; 1613-9089
• DOI: 10.1007/s10330-010-0715-1

Objective： We studied the effects of Wortmannin （WM） on the proliferation and apoptosis of leukemia cells, and explore the possible mechanisms. Methods： The human myeloid leukemia cell line K562 was treated with different concentrations of WM, and then detected the activity of the cell proliferation by MTT assay, comet tail formation of cell DNA damage phenomenon by single cell gel electrophoresis, cell apoptosis byAnnexin V-FITC/PI double staining and the expression levels of total Akt, phoshorylated Akt, NF-KB and protein in K562 cell by Western blotting, RT-PCR test before and after WM. Results： WM inhibited cell proliferation of K562 in a concentration-dependent manner, with IC50 value for 24 h being 25 nmol/L. WM induced apoptosis of K562 cells in a concentration-dependent manner, and could induce the breakage of DNA strand of K562 cell. The rate of DNA tail and the tail length of experimental groups were significantly higher than that of control group. WM may inhibit the expression of phosphorylated Akt and NF-KB protein in a dose-dependent manner in both the protein and gene levels, but no significant effect on total Akt protein. Conclusion： WM inhibited cell proliferation and induced apoptosis in K562 and concentration-dependent manner. The possible mechanism may be involved in the regulation of survival signaling pathway, such as PI3K/Akt/NK-KB.